Does How We Lose Weight Matter?

The response to GLP-1 drugs has exposed a strange tension in how we think about weight loss. On one side, people who have lost weight through diet, exercise, and changes to their lifestyle can sometimes act as though they earned their result in a way that people using medication did not. On the other side, criticism of drugs like semaglutide or tirzepatide is often dismissed as moral judgment, as though the only reason someone could prefer weight loss without medication is because they think fat people should suffer for becoming fat. I don't think either position gets very far.

There has always been a tendency to treat body weight as evidence of character, as though being lean proves discipline and being fat proves some kind of personal failure. I don't think that is a useful way to look at people, and I'm not interested in arguing that somebody who loses weight without medication is therefore a better person than somebody who uses a GLP-1. At the same time, I don't think it follows that the way somebody loses weight is irrelevant.

Part of my bias here is obvious. I work in an industry where behavior matters. I've also gone through the process of losing weight without medication, so I understand that I am naturally going to place value on what that required from me. But even after accounting for that bias, I still think there is something different about changing the conditions and behaviors that contributed to a problem compared with using a drug that allows you to reach a similar outcome while leaving many of those things unchanged. That difference is where I think some of the conversation about morality gets confused.

Morality has to show up somewhere in behavior. We generally judge honesty by whether someone tells the truth, responsibility by whether someone takes responsibility, courage by what somebody does in situations where courage is required. These things aren't simply ideas somebody carries around internally. They are expressed through behavior, and repeated behavior eventually contributes to the kind of person somebody becomes.

Weight loss can require some of those same qualities. You may have to regulate what you eat when you would rather keep eating, change the food you keep around the house, move when you don't particularly feel like moving, learn how food affects you, prepare meals differently, tolerate hunger occasionally, build routines, recover from mistakes, and continue doing those things for long enough that the way you live actually changes. I don't think doing those things makes you morally superior to somebody else, but I do think those behaviors can develop qualities that I respect.

That is why, if you give me two hypothetical people who both need to lose 100 lbs, I don't view their paths as interchangeable simply because the scale eventually shows the same number. One person may spend a year or two changing how he eats, becoming more active, learning how to train, changing what food is available around him, learning how much he actually needs to eat, dealing with hunger and setbacks, and eventually reaching a point where his daily life looks very different from the one that helped him become obese. The other person may begin taking a GLP-1, experience a large reduction in appetite, eat substantially less without having to fight the same degree of hunger, lose the same 100 lbs, and make relatively few changes to the rest of his life.

The second person still lost the weight, and the result is real. He may improve his blood pressure, glucose levels, mobility, sleep, and other parts of his health as a consequence. I don't think any of that should be dismissed. I still respect what the first person did more, and I don't think saying that requires me to believe the second person has less human worth. I'm judging what each person had to do in response to the problem, and equal human worth doesn't require me to admire every way of solving a problem equally.

The complication is that those aren't the only two possibilities. Somebody could use a GLP-1 while completely changing the way he eats, beginning to exercise, becoming more active, and learning how to manage his health in ways he never had before. Somebody else could use the drug as the entire strategy. Those seem meaningfully different, which is why I have much less of a problem with the first person than the second. What concerns me most is when the drug becomes a replacement for participating in your own health.

GLP-1 drugs make this question particularly interesting because they are sometimes discussed as though they are simply another tool. The argument usually goes something like this: we don't criticize people for using washing machines instead of washboards, calculators instead of doing arithmetic by hand, or cars instead of walking everywhere, so why should we criticize someone for using a medication that makes losing weight easier? I understand the comparison. Human beings use technology constantly to remove unnecessary difficulty from our lives. I don't think making something easier automatically makes it worse, and I don't think difficulty has some magical moral value.

The washing-machine comparison breaks down for me because washing clothes is an external task. Human beings don't have a physiological capacity for washing clothes that we need to maintain for our health. Using a machine to wash my clothes doesn't change the way my appetite functions, affect the amount of muscle I carry, alter my cardiovascular fitness, change my ability to regulate food intake, or make my health dependent on continued use of the machine. A GLP-1 is different because it acts on physiology.

Drugs such as semaglutide and tirzepatide alter the biological signals involved in appetite and satiety, which can make it considerably easier for someone to eat less. That can be extremely useful, but it also means the medication is participating directly in a regulatory process that the person would otherwise have to manage through some combination of physiology, behavior, and environment. The medication isn't simply removing unnecessary labor from an unrelated task.

I feel like this matters because I keep coming back to health as a capacity rather than simply a collection of outcomes. Body weight is one outcome. Blood pressure, glucose, cholesterol, and body fat are outcomes. They matter, but I don't think they completely describe whether somebody is healthy. I also care about what the person is capable of regulating and maintaining, what his body can tolerate, how well he functions, how he responds to stress, whether he can move and produce force, and whether the behaviors that support those things have actually become part of his life. Two people can therefore arrive at the same body weight while arriving there with different capacities.

The comparison I keep thinking about comes from training. Imagine two people who can both bench press 405 pounds. One trained naturally for years to reach it. The other used large amounts of anabolic steroids and reached the same strength much faster. Both still benched 405 pounds. The bar doesn't care how they got there. But most people who understand training would hesitate to say that the two paths tell us exactly the same thing.

The person using anabolic drugs received a pharmacological advantage that changes the rate at which muscle and strength can be gained. They may also be accepting physiological risks associated with those drugs. The faster increase in muscular force can create its own problems if other tissues haven't adapted at the same rate, and if the drugs are removed, the conditions supporting the result change. None of that means the strength is imaginary. It means the result cannot be separated completely from the method that produced it.

I think weight loss works in a similar way. If somebody changes what he eats, becomes more active, gains or preserves muscle, improves aerobic capacity, restructures his food environment, and develops greater control over his own behavior, those changes have effects beyond the number he sees on the scale. If somebody reaches the same scale weight primarily because a medication has suppressed his appetite enough for him to eat less, that doesn't make the weight loss fake. It means I don't automatically consider the two states identical simply because the outcome we are measuring happens to be the same. The process changes the person and the organism along the way.

This is also where my broader concern about our relationship with technology comes in. Humans have created an environment that makes many of the behaviors required for health increasingly optional. We can avoid movement almost completely. We can have food delivered without leaving the house. Food can be available continuously, in forms specifically designed to be easy to eat and difficult to stop eating. We can stay indoors for most of the day, remain under artificial light late into the night, sit for hours at work, and structure most of daily life around convenience.

Many behaviors that would once have occurred as a normal consequence of being alive now have to be deliberately reintroduced. In that sense, I sometimes think of modern life as a kind of captivity of our own construction. I don't mean that literally, and I don't think modern life is uniformly bad. I mean that we have engineered away many of the constraints and physical demands that human physiology developed within, and then we increasingly rely on additional technology to compensate for some of the problems that emerge from the environment we created.

GLP-1s can fit into that pattern. If somebody lives in an environment where he repeatedly overeats, moves very little, has constant access to highly palatable food, sleeps poorly, and has become obese, a drug that substantially reduces appetite may help him lose a large amount of weight without requiring him to alter many of those conditions. That may still make him medically better off.

There may also be people for whom medication is the best available option. Someone with severe obesity who has repeatedly tried to lose weight, has significant health problems, and is struggling to function may reasonably decide that medication gives him a chance to get out of a situation he has not been able to change on his own. I don't think refusing useful treatment simply to prove that you can do something without help is automatically virtuous.

My concern begins when pharmaceutical compensation becomes the first or only answer to a problem that could reasonably involve changing the conditions producing it, particularly when those changes would improve several parts of someone's health at the same time. The further we move toward needing an external pharmaceutical input to perform a regulatory function we would otherwise have to develop or maintain ourselves, the more dependent that outcome becomes on the intervention.

That dependence becomes relevant when we ask what happens if the intervention disappears. GLP-1 medications can produce substantial weight loss while they are being used, but many people regain weight after stopping them. That doesn't necessarily mean they failed morally or learned nothing. Weight loss itself can produce biological pressures toward regain, including increased hunger and changes in energy expenditure. Still, if the person's environment, routines, food choices, activity, and ability to regulate intake remain mostly unchanged, then removing the thing that was suppressing appetite predictably leaves many of the original conditions in place.

That is why I hesitate to describe medication alone as a complete solution. It can solve part of the problem. It can reduce body weight and improve some of the consequences associated with obesity. It may create enough space for someone to begin changing the rest of his life. What it cannot guarantee is that the person develops the capacities required to maintain those changes without the drug.

That brings me to the argument that obesity is a disease. I understand why people use that language. Excess body fat can contribute to real physiological dysfunction and disease, and severe obesity can clearly impair someone's ability to function. I also don't think the fact that a condition responds to changes in environment automatically proves that it isn't a disease. Plenty of medical conditions are caused or aggravated by environmental exposures.

Where I become hesitant is when the disease label is used as though it settles the question of causation or removes behavior from the discussion. If somebody becomes obese in an environment with constant food availability, little required movement, poor sleep, highly processed food, and routines that encourage overeating, then those conditions still belong in the explanation. Genetics can affect how susceptible someone is to that environment. Physiology can make losing weight harder for one person than another. None of that makes the environment or the person's behavior irrelevant.

I also don't think every person with excess body fat is necessarily in the same physiological state. Someone can carry more body fat while remaining relatively functional and metabolically healthy for a period of time, while someone else may already have impaired glucose control, sleep apnea, joint problems, limited mobility, cardiovascular disease, or other consequences associated with obesity. Simply placing both people under one label doesn't tell me everything I need to know about their health.

The issue of suffering sits underneath a lot of this too. Critics of people who prefer weight loss without medication sometimes describe that preference as though they believe weight loss should be painful. The implication is that people want someone with obesity to grind through misery as punishment for having gained weight in the first place. I don't believe that, and I also think "suffering" gets used too loosely in these discussions.

Eating less than you want to eat can be uncomfortable. Going for a walk when you would rather sit down can be uncomfortable. Training can be uncomfortable. Learning to cook when ordering food is easier can be inconvenient. Saying no to something you want in the moment can be frustrating. Changing a familiar way of living can feel much harder than continuing it, but that's different from saying the person is being harmed by the process.

Meanwhile, remaining significantly overweight can involve its own form of suffering: aching joints, difficulty moving, getting winded easily, poor sleep, reduced physical capacity, metabolic disease, and feeling trapped in a body that doesn't function the way you want it to. People can become comfortable with what they know even when what they know is making them miserable. The discomfort of changing may feel worse initially because it is unfamiliar.

I don't think discomfort automatically has moral value. Making something harder for no reason doesn't improve it. Starving yourself unnecessarily isn't admirable. Training through an injury isn't admirable. Refusing medication when you genuinely need it doesn't prove character. I place value on challenge when going through it develops a capacity you actually need.

That is where my view of health starts to shape how I think about all of this. You don't simply acquire health once and then possess it regardless of what you do. You are born with a body that has an enormous amount of biological capacity, and what happens to that capacity over time is influenced by age, genetics, environment, disease, and behavior. Some capacities decline eventually because aging is real. Others can improve considerably through what you do.

You can become stronger. You can improve aerobic fitness. You can improve insulin sensitivity. You can gain muscle and bone. You can improve movement. You can become better at regulating your behavior and arranging your environment so that those behaviors are easier to maintain. I think there is value in deliberately developing and maintaining those capacities while you are able to.

That is why I have much less of a problem with somebody who uses a GLP-1 with the expressed intention of changing his lifestyle at the same time. The medication may reduce appetite enough for him to get traction. Losing weight may allow him to move without pain. Improved mobility may allow him to start exercising. Training may help him build muscle and improve cardiovascular fitness. Learning how to eat differently while the medication makes appetite easier to manage may give him skills that remain useful later. In that situation, the drug is participating in a larger process.

Where I become uncomfortable is when the intervention becomes the process. If somebody's entire approach to weight loss becomes taking something that makes him eat less while the behaviors, environment, and physical capacities surrounding the problem remain essentially untouched, then I think we have started confusing improvement in one measurable outcome with health more broadly.

That doesn't mean the person is bad, the weight loss is illegitimate, or the medication has no medical value. It means I place more value on a process that leaves somebody increasingly capable of participating in and regulating his own health than on one that leaves those capacities largely undeveloped and makes the result heavily dependent on an outside intervention.

There is probably a moral component to that belief because agency, responsibility, behavior, and character are moral questions to some degree. I don't think that requires condemnation. I can respect somebody as a person, understand why he chose medication, agree that the medication improved his condition, and still think the way we choose to respond to problems contributes to the kind of person we become.

How we repeatedly solve problems shapes us, although I don't think one choice tells me everything about somebody. Sometimes the right solution is technological or pharmaceutical because the problem exceeds what we can reasonably handle ourselves. Sometimes outside intervention gives someone the ability to begin doing things he previously couldn't do. I don't want a philosophy so rigid that it cannot account for those situations, but I also don't want a philosophy of health where every human capacity can be replaced by an external intervention as long as the numbers look better afterward.

If the behaviors required to maintain health are still within our reasonable capacity, I think there is something worth preserving in continuing to develop and exercise them. That doesn't make every pharmaceutical intervention wrong, but it does change what I think the intervention should be doing within the larger process of becoming and remaining healthy.

Cardio and Lifting: How to Do Both Without Killing Your Progress

There is an old idea in strength training that cardio kills your gains. Like most absolutes in fitness, it takes something that can happen under certain conditions and turns it into a rule that supposedly applies to everyone. Cardio does not automatically prevent you from getting stronger or building muscle, and for most people there is no reason they cannot improve their cardiovascular fitness while continuing to make progress in the weight room. The problem begins when the cardio you are doing creates enough fatigue, muscular stress, or recovery demand that it starts compromising the lifting responsible for the result you actually care about.

This is why the first question should not be whether cardio is good or bad for muscle growth. The better question is why you are doing cardio in the first place. Someone walking to increase energy expenditure during a fat-loss phase, someone doing moderate aerobic work for cardiovascular health, and someone preparing for a marathon are all technically “doing cardio,” but they are solving completely different problems. The purpose of the cardio should determine the modality, frequency, intensity, and amount you use, as well as how much of your recovery you are willing to dedicate to it.

Why Are You Doing Cardio?

For someone primarily focused on body composition, cardio is usually a tool for increasing activity and energy expenditure. In that situation, there is very little reason to immediately choose the hardest form available. Daily walking, incline treadmill work, easy cycling, or other low-intensity activity can increase expenditure while creating relatively little additional fatigue. For some people, simply increasing daily steps will accomplish what they need. If more activity is necessary, adding 20–30 minutes of low-intensity cardio after lifting sessions is a reasonable place to start and can be increased only when the goal actually requires it.

Cardio for general health serves a different purpose. Here the objective is to improve cardiovascular fitness and aerobic capacity rather than simply burn additional calories. Regular moderate aerobic work that can be repeated and recovered from makes sense, and something in the range of 20–40 minutes two or three times per week can be a practical starting point. This work does not need to become another maximal training session. HIIT can have a place, but harder work is not automatically more useful when the desired adaptation can be achieved with a lower recovery cost.

Endurance performance changes the conversation again because specificity now matters. If you want to become a better runner, you eventually have to run enough to improve at running. If you are preparing for a marathon, the volume, frequency, and specificity of the endurance work have to become large enough to drive those adaptations. At that point, cardio is no longer simply supporting your lifting program; it has become one of the primary goals of the training phase. Some reduction in the rate of hypertrophy may come with that shift, but that is not necessarily a programming mistake. It is the predictable cost of prioritizing a different quality.

Where the Interference Actually Comes From

Combining resistance training and endurance work is commonly referred to as concurrent training, and the potential reduction in strength or hypertrophy adaptations is usually called the interference effect. This has often been interpreted to mean that cardio somehow burns muscle or shuts down muscle growth, but that is an overly dramatic way to describe what is usually a much simpler problem. Concurrent training generally does not appear to produce a large reduction in whole-muscle hypertrophy under normal conditions, although some forms of aerobic work seem to create more interference than others. The practical issue is usually the total amount of stress being accumulated and whether the person can continue recovering well enough to train productively.

Three variables are especially useful when thinking about that stress: frequency, intensity, and modality. The more often you perform cardio, the harder those sessions are, and the more muscular damage or impact the modality creates, the more likely it is to compete with the resistance training you are trying to prioritize. There is no universal number of sessions where cardio suddenly becomes excessive because recovery capacity differs from person to person. Someone sleeping well, eating enough, and performing relatively low-fatigue aerobic work may tolerate a considerable amount. Someone dieting aggressively, training legs hard several times per week, sleeping poorly, and adding frequent running sessions may reach their limit much sooner.

Intensity changes the cost of the work considerably. Walking, incline treadmill work, and easy cycling generally create relatively little fatigue, which is why they can usually be performed more frequently. Hard intervals and sprint work are different. They may be more time-efficient, but they also create a larger recovery demand and overlap more heavily with the high-intensity muscular work already being performed in the weight room. If the purpose of cardio is simply to increase energy expenditure during a body-composition phase, turning every session into HIIT often creates more fatigue than the goal requires.

Modality matters for the same reason. Walking and cycling generally create less impact and eccentric muscular stress than running. Running is not inherently bad for hypertrophy, but it tends to be more expensive from a recovery standpoint, particularly as volume and intensity rise. If someone is preparing for a race, that cost is necessary because running is the adaptation being pursued. If someone is simply trying to burn a few extra calories while maximizing lower-body hypertrophy, choosing a lower-cost modality is usually the more sensible option. The principle is simple: use the least costly tool that still accomplishes the job.

The Mechanism Is Probably Less Complicated Than It Sounds

A great deal of discussion around concurrent training has focused on molecular signaling. One of the better-known explanations was that endurance exercise activates AMPK and other signaling pathways associated with aerobic adaptation, which could suppress mTOR signaling and interfere with the muscle-building response to resistance training. That explanation is interesting, but the evidence has not supported such a clean relationship. Aerobic and resistance exercise can be performed in relatively close proximity without necessarily producing the kind of suppression of anabolic signaling that the original hypothesis predicted.

There are other molecular explanations that remain possible, but from a coaching standpoint there is a much simpler explanation that matters more: fatigue reduces what you are able to do in the gym. Resistance training needs to provide enough tension and effort to stimulate the muscle fibers you are trying to grow. If hard cardio leaves you fatigued before your next lifting session, you may use less weight, perform fewer reps, produce less force, or struggle to recruit the same high-threshold motor units you otherwise could. An isolated bad workout does not matter much, but if cardio repeatedly reduces the quality of the resistance-training stimulus, the accumulated result can be less hypertrophy than you would have achieved otherwise.

That is the useful way to think about the interference effect. Cardio does not have to directly destroy muscle to interfere with muscle growth. It simply has to make the training responsible for building that muscle consistently worse.

If Muscle Is the Goal, Protect the Lifting

Once the priority is clear, the order of training becomes fairly straightforward. If size and strength are the primary goals, lifting should receive the best of your energy and recovery. That generally means resistance training comes first when lifting and cardio need to happen on the same day. Low-intensity work can often be performed immediately afterward because it creates relatively little additional fatigue. If the cardio session is harder, separating the two sessions by several hours can be useful so there is time to eat, hydrate, and regain some performance capacity before training again.

The exact number of hours is not magical. Something around three to six hours is a reasonable practical guideline when the second session is more demanding, but the larger principle is simply to avoid asking the body to perform two difficult sessions back-to-back when there is no need to do so. If the goal is hypertrophy, the resistance-training session is the one you want to protect.

There is also a difference between separating training sessions and separating training days. Coaches sometimes alternate lifting and cardio throughout the week because it appears to create more recovery between each type of training. In reality, this can leave the same muscles working almost every day. A lower-body session on Monday, running on Tuesday, another leg workout Wednesday, and more conditioning Thursday technically separates the modalities while providing very little actual recovery for the legs.

In many cases, it makes more sense to consolidate the stressors. Place cardio on the same days as lifting when appropriate, perform the lifting first, and then leave complete recovery days afterward. This concentrates the workload into fewer days and gives the muscles and nervous system longer uninterrupted periods to recover. For someone whose main goal is hypertrophy, that can be a much cleaner way to organize concurrent training than spreading some form of lower-body stress across the entire week.

How Much Cardio Should You Actually Do?

There is no single cardio prescription because the amount should come from the goal rather than from the belief that more exercise is automatically better. If body composition is the priority, start with daily movement and use steps as the first lever. If additional expenditure is needed, add 20–30 minutes of low-intensity work after lifting sessions and assess what happens before doing more. If fat loss is already progressing at the desired rate, adding more cardio simply because it is available does not accomplish anything useful.

For general health, the goal is to establish a consistent aerobic base that complements resistance training. Moderate aerobic sessions a few times per week are enough to provide meaningful cardiovascular work for many people without turning the entire program into conditioning. Higher-intensity intervals can be added if there is a reason for them, but they should not automatically replace lower-intensity work simply because they feel more difficult.

For endurance performance, the required amount becomes much more specific to the event. More running, cycling, intervals, or longer sessions may be necessary, and eventually that increased workload has to be reflected elsewhere in the program. Resistance-training volume may need to come down, lower-body training may need to be reorganized, and expectations for hypertrophy may need to change during that phase. Training resources are finite, so increasing the priority of one quality inevitably changes how much can be invested in another.

You Can Improve Both, but One Has to Take Priority

This is ultimately the part of concurrent training that people tend to avoid. You can improve multiple qualities at the same time, but you cannot assume that every quality can be maximized simultaneously. If bodybuilding is the goal, lifting should drive the program and cardio should support body composition, health, or conditioning without consistently compromising resistance-training performance. If you decide to prepare for a marathon, endurance training becomes the primary focus and hypertrophy takes a secondary role for that period.

Neither choice is better. They simply require different programs. The problem begins when someone says muscle growth is the priority while training like an endurance athlete, or says endurance performance is the priority while refusing to give it enough training volume because they are afraid of sacrificing any hypertrophy. The goal has to determine what receives the majority of your time, effort, and recovery.

The simplest way to know whether you have found the right balance is to watch the thing you are trying to protect. If your loads, repetitions, execution, and recovery continue improving while cardio is in the program, there is little reason to assume the cardio is meaningfully interfering. If your legs are constantly fatigued, performance begins to fall, soreness never resolves, or progression stalls after cardio volume increases, the dose has probably exceeded what you can currently recover from. At that point, reduce the frequency, lower the intensity, choose a less demanding modality, reorganize the week, or improve the recovery supporting the training.

Cardio and lifting are not natural enemies. The problem is usually trying to do more work than the goal requires or more work than the athlete can recover from. Determine why the cardio is there, choose the modality that accomplishes that goal with the lowest necessary recovery cost, give the priority training the best of your performance, and adjust the total dose according to what your body is actually showing you. You can improve both cardiovascular fitness and muscle mass. You simply have to be clear about which one leads when the demands begin to compete.

Reimagining the Meaning of Health

When people talk about health, they often assume it's a straightforward and easily definable concept: either you're healthy or you're not. But the moment you try to explain what health actually is, the idea becomes much less clear. Is it how you feel? Is it how your body performs? Or is it something broader that includes how you live, think, and function in the world?

There is a recognized field called the philosophy of medicine, or the philosophy of health and disease, but there isn't one dominant, universally accepted philosophy of health in the same way there are recognizable schools like Stoicism, utilitarianism, existentialism, or pragmatism. The closest thing we have to an official global definition comes from the World Health Organization, which defines health as “a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.”

The WHO definition falls short as a complete philosophy of health and instead acts more like an ideal. It says health is more than “not being sick,” which is important, but it doesn't fully explain how a person should live, what tradeoffs matter, what the body is for, how much responsibility belongs to the individual versus society, or how to judge health when someone has pain, disability, disease, aging, trauma, or chronic stress.

A better way to frame it is this: there are many different ways to think about health, but no single definition or perspective fully captures what it means in practice.

The main reason is that health sits between biology, morality, culture, medicine, politics, economics, and personal meaning. It isn't purely objective, nor is it purely subjective. A blood marker can be objectively abnormal, but whether someone is healthy cannot always be reduced to that marker. A person can have perfect labs and still be miserable, addicted, socially isolated, weak, anxious, and unable to function. Another person can have a chronic condition but live with strength, purpose, connection, resilience, and high function.

This is why philosophers and physicians distinguish between disease, illness, and sickness. Disease can refer to biological dysfunction, illness to the lived experience of being unwell, and sickness to the social role or recognition of being unwell. Those categories overlap, but they are not identical. Someone can have disease without feeling ill. Someone can feel ill before a diagnosis appears. Someone can be treated socially as sick even when their deeper problem is environmental, psychological, relational, or behavioral.

The major split is usually between two views.

One view is the biological view. In this view, health means normal biological functioning. This is associated with thinkers like Christopher Boorse, who treated health as a theoretical biological concept. The strength of this view is that it keeps health grounded in physiology instead of preference, ideology, or vague wellness language. The weakness is that normal function doesn't fully capture pain, meaning, adaptation, environment, social conditions, or human flourishing. You could describe this view as functional, in the sense that it focuses on whether the system is operating as it is supposed to.

This view becomes more complicated when applied to aging, disability, or chronic conditions. If health is defined only by normal biological functioning, then many predictable features of aging or disability can be treated as straightforward defects. But that misses something important: a person may have limitations, adaptations, or medical realities and still possess a high degree of health in the lived sense if they can function, adapt, participate, and pursue a meaningful life.

The other view is the holistic view. In this view, health is about the person’s ability to live well, pursue meaningful goals, participate in life, and adapt to challenges. This includes thinkers like Georges Canguilhem and Lennart Nordenfelt, and it fits better with real life because health isn't only about whether the organism is working, it's also about whether the person can function in the world they inhabit. A useful parallel term here is integrative or adaptive, since this view looks at how different factors come together and balance to make health possible, rather than focusing only on isolated biological function.

That is why more recent definitions have moved toward health as adaptability. A widely cited proposal in the British Medical Journal defines health as “the ability to adapt and to self-manage” in the face of physical, social, and emotional challenges. That gets closer because health isn't a perfect static state — it's dynamic, requiring the capacity to respond.

So if we had to build a generally recognized philosophy of health from the broad consensus, it would probably be something like this:

Health is the cultivated capacity to function, adapt, and pursue a meaningful life through the integration of body, mind, behavior, environment, and community.

Or put more simply: Health is the capacity to live well in reality.

It's not endless optimization, perfect biomarkers, visible leanness, or total control. It also isn't static or universally experienced in the same way across all people, stages of life, or environments. A real philosophy of health would probably rest on a few core principles that account for both its biological realities and its lived complexity.

First, health is functional. The body should support life, not become the entire purpose of life. Strength, mobility, energy, sleep, digestion, cognition, and emotional regulation matter because they increase someone’s ability to act.

Second, health is adaptive. A healthy person is not someone who never experiences stress, illness, pain, or disorder. A healthy system can respond, recover, reorganize, and continue functioning. This is why the ability to adapt and self-manage is such a useful model.

Third, health is multidimensional. Physical, mental, social, and environmental health cannot be fully separated. The WHO definition gets this part right by refusing to define health as merely the absence of disease.

Fourth, health is both personal and collective. Individuals have responsibility for their habits, but people do not choose all of their conditions. Food access, income, stress exposure, education, neighborhood safety, healthcare access, and culture shape health. One criticism of the self-management model is that it can accidentally blame people who have fewer resources or lower capacity to adapt.

Fifth, health isn't the same as morality. Being healthy doesn't make someone virtuous, and being sick doesn’t make someone a failure. This matters because modern wellness culture often turns health into a moral hierarchy.

Sixth, health exists to support a good and meaningful life. The purpose of health is to expand what life allows: to love, work, think, create, endure, contribute, enjoy, and participate.

Part of what makes a philosophy of health so difficult is that health is too broad to belong to one discipline. Medicine wants diagnosis. Biology wants function. Public health wants population outcomes. Psychology wants resilience and behavior. Philosophy wants meaning and value. Fitness wants performance and body composition. Spiritual traditions often want wholeness, discipline, or harmony.

But the closest modern synthesis would be this:

Health centers on capacity rather than perfection. It reflects a person’s ability to meet life with enough physical function, mental clarity, emotional resilience, social connection, and environmental support to pursue a meaningful existence.

That is the most defensible starting point for a philosophy of health, but it still feels incomplete on its own. A philosophy of health cannot stop at defining what health is in theory; it also has to extend into practice. It needs to account for how health is actually built over time, how it's maintained, how it breaks down, and how it can be restored when it is lost.

Health, to me, isn't just the absence of disease, and it isn't something that can be fully understood through lab numbers, body fat percentage, or appearance alone. It is a state of bodily function, movement quality, emotional steadiness, and physiological resilience that gives a person the freedom, confidence, and capacity to live the life they want.

Someone can look fit and still be unwell. Someone can have impressive numbers and still lack energy, stability, strength, clarity, or peace. Real health is when the body works well, adapts well, and supports a high quality of life without constant limitation, discomfort, or dependency.

This is where my view becomes more specific. I believe health is built by living in alignment with what human beings fundamentally need. That includes movement, sunlight, connection, quality food, sleep, stress management, purpose, time in nature, and daily habits that work with our biology rather than against it.

I don't see the body as a machine that simply needs to be medicated whenever symptoms appear. I see it as a living system that needs to be understood, supported, and respected. Symptoms are not random inconveniences to suppress. They are often signals that something deeper may be out of order. That does not mean medicine has no place. It means medicine should not be the only lens. Real health, in my view, comes from addressing causes rather than only managing consequences.

This also means that health cannot be separated from behavior. The body is shaped by what it repeatedly experiences. The food someone eats, the way they move, the sleep they get, the stress they carry, the relationships they maintain, the light they see, the environments they inhabit, and the standards they live by all become information to the body. Over time, those repeated inputs either support function or erode it.

That is why I do not view health as a temporary intervention or a short-term fix. I see it as a way of living. It is built through sustainable habits, standards, and identity, not through quick fixes or temporary bursts of motivation. A diet only matters if it can actually be lived. A training plan only matters if it can be recovered from and repeated over time. A strategy only matters if it helps someone become the kind of person who can carry it forward.

Therefore, health is not just about what a person does once in a while. It is about what they repeatedly choose, what they value, and who they're becoming.

But health should also lead somewhere. It is not the final goal in itself. It is the foundation that gives a person the ability to act, choose, lead, and live with greater purpose. Good health allows someone to be more present, more capable, and more fully themselves. That is part of why confidence in one’s body matters. It reflects freedom, self-respect, and the ability to move through life with strength and agency.

In this sense, health is both biological and philosophical. It is biological because the body has real needs, real limits, and real consequences when those needs are ignored. But it is philosophical because the point of health is not merely to survive, optimize, or avoid disease. The point is to create the capacity for a fuller life.

Health is not perfection. It isn't a number, a look, a supplement stack, or a temporary state of discipline. Health is the cultivated capacity to live well in reality. It is the condition of the body and mind that allows a person to meet life with strength, adaptability, clarity, and purpose.

And if there is a philosophy of health worth building around, I think it's this:

The body is not the destination. It is the foundation. Health is the practice of building that foundation well enough that life can be lived with more freedom, presence, and meaning.

The Toxic Burden We Pass Down

Toxic exposure is usually discussed as an individual issue. A person is exposed to a chemical, heavy metal, pollutant, or environmental stressor, and the concern is how that exposure affects their health.

But the deeper concern is that toxic exposure may not stop with the individual.

The amount of a toxin a person is exposed to at any point in their lifetime may influence future generations through epigenetic changes. This does not necessarily refer only to a person’s present toxic load, or total body burden. The concern is that exposure itself may leave biological information that can be passed forward through the epigenetic code.

Epigenetics refers to changes in how genes are expressed. It does not change the underlying DNA sequence, but it can influence which genes are turned on or off, and how strongly those genes behave. In this way, the environment can affect biology in ways that may extend beyond one lifetime.

That means a toxin may not only affect the person directly exposed to it. It may also affect their children, grandchildren, and future descendants.

The concerning part is that future generations may not simply inherit the same level of vulnerability. They may become more sensitive to the same exposure.

For example, scientists have found that when the first generation of frogs is exposed to a given amount of mercury, they display a certain level of injury or mutation. But the damage caused by that same amount of heavy metal doubles in the second generation and doubles again in the third generation, until none of them survive.

Instead of gaining tolerance, which can happen in some biological processes, they developed a dramatically greater intolerance with each generation.

That matters because it challenges the way we usually think about adaptation. We often assume that repeated exposure might make an organism stronger or more capable of handling the stressor. But with certain toxins, the opposite may happen. The exposure may alter gene expression in a way that increases vulnerability rather than resilience.

This is the idea of generational body burden.

A toxic exposure may affect the parent, but it may also change how future generations respond to environmental threats. The same amount of toxin may cause more harm later because the inherited epigenetic pattern has made the organism less capable of tolerating it.

That increased sensitivity can make future generations weaker in several ways. They may have a harder time fighting off environmental threats. They may struggle more to recover from health challenges. They may also have a reduced ability to normalize or compensate for genetic defects.

This does not mean every exposure automatically creates permanent damage in every descendant. It does mean that toxic exposure should be taken more seriously than a single-lifetime model allows.

The body is not isolated from ancestry. Health is shaped by the environments we live in, but also by the biological history passed down to us. The exposures of previous generations may influence how resilient or vulnerable the next generation becomes.

This also means that reducing toxic exposure matters beyond personal health. The choices we make around food, water, chemicals, heavy metals, air quality, personal care products, and environmental burden may influence more than our own biology.

They may shape the biological starting point of the people who come after us.

That is why detoxification and toxic load should not be treated as trendy wellness language. The body carries information from its environment. Some of that information may be passed forward. If toxic exposure can influence gene expression across generations, then lowering exposure becomes part of a larger responsibility.

We are not only managing our own body burden.

We may also be influencing the burden inherited by future generations.

What You Put on Your Skin Still Enters Your Body

Most people pay attention to what they eat, drink, and breathe, but they often forget that the skin is also an entry point into the body.

When you put chemicals, makeup, skincare products, oils, soaps, hair products, or other substances on your skin, some of those compounds can be absorbed through the skin and enter circulation. This is one reason personal care products deserve more attention than they usually get.

A simple example often used to explain this is a garlic poultice. A poultice is a soft, moist mass of some substance applied to the body for a medicinal purpose and kept in place with a wrap of cloth or plastic. If garlic is applied to a baby’s feet as a poultice, it has been said that the smell can appear on the breath shortly after. Whether or not that example is precise in every case, the larger point is that substances placed on the skin can influence the body beyond the surface.

Medical science already understands this principle. Transdermal medications have been used for decades. Medicinal patches are applied to the skin when oral delivery is not ideal, when absorption through the digestive tract is poor, or when a steady delivery of medication is preferred.

That alone should change the way we think about skincare and personal care products.

The skin is not an impenetrable wall. It is a living, responsive barrier. It protects the body, but it can also absorb certain substances. The degree of absorption depends on the compound, the condition of the skin, the area of application, the amount used, and how often it is applied.

What makes skin absorption especially important is that substances absorbed through the skin do not go through the liver first in the same way swallowed substances do. When you eat or drink something, it generally passes through the digestive system and then through the liver before reaching the wider bloodstream. This is part of what is called first-pass metabolism.

When something is absorbed through the skin, it can enter circulation more directly, do what it is going to do, and then be filtered by the liver later.

That matters because personal care products are not occasional exposures for most people. They are daily exposures. Makeup, lotions, sunscreen, deodorant, shampoo, conditioner, soap, fragrance, shaving products, and skincare formulas can create repeated contact with chemical compounds over time.

The concern is not that every product is automatically dangerous. The concern is that most people use these products casually without thinking of them as part of their total toxic load.

If something is applied to the skin once, the exposure may be small. But if multiple products are used every day for years, the cumulative exposure becomes more relevant. The body has to process what it absorbs.

This is why personal care products should be treated with the same level of awareness as food. The skin may be external, but what you place on it does not necessarily stay external.

A better approach is to simplify where possible. Use fewer products. Choose cleaner formulas when you can. Avoid unnecessary fragrance. Pay attention to ingredients. Remember that the body is exposed not only through food and air, but also through the products used on the skin every day.

Your skin protects you, but it also connects you to the environment.

That means what you put on your body still matters to what happens inside your body.

How Blue Light at Night Affects Blood Sugar

Excess blue light does more than affect sleep. It may also contribute to inflammation and mitochondrial dysfunction, largely because of its impact on glucose control.

This matters because light is not just something we use to see. Light is biological information. The body uses light to help regulate circadian rhythm, hormone timing, metabolism, sleep, and energy production. When the wrong light comes at the wrong time, the body can receive the wrong signal.

Blue light during the day, especially from the sun, can be useful because it helps reinforce wakefulness and circadian timing. But blue light in the evening can create a different effect. Evening exposure to blue light has been shown to influence glucose levels, leading to higher blood sugar and increased insulin resistance.¹

That means your blood sugar may stay higher than it should, while your body becomes less effective at moving that sugar out of the bloodstream.

Insulin resistance is the condition where the body does not respond to insulin as well as it should. Insulin’s job is to help move glucose from the blood into the cells, where it can be used or stored. When insulin sensitivity decreases, blood sugar remains elevated more easily, and the body has to work harder to maintain normal glucose control.

Over time, this can become a problem for metabolic health.

The result is that excessive artificial light at night may increase the risk of weight gain and contribute to the development of type 2 diabetes. Research has also raised the question of whether artificial light at night contributes to the worldwide obesity pandemic.²

This is important because most people think about blue light only through the lens of sleep. They know screens at night may make it harder to fall asleep, but they may not realize that nighttime light exposure can also affect metabolism.

The body expects a rhythm: brighter light during the day and darkness at night. That rhythm helps coordinate the systems that regulate energy, blood sugar, hormones, and cellular function. When artificial light extends the “day” into the evening, the body may continue operating as if it should remain alert and metabolically active.

That mismatch can affect glucose regulation.

If evening blue light causes blood sugar to rise and contributes to insulin resistance, then nighttime screen use, bright indoor lighting, and artificial light exposure may be more significant than people realize. This is especially relevant for people already struggling with weight gain, poor sleep, blood sugar instability, or metabolic dysfunction.

The solution does not need to be complicated. The goal is to respect the body’s natural light-dark cycle.

During the day, get bright natural light. In the evening, dim the lights. Reduce screen exposure close to bed. Use warmer lighting when possible. Avoid bright overhead lights late at night. Give the body a clearer signal that the day is ending.

This is not only about sleeping better. It is about helping the body regulate glucose, insulin, inflammation, and mitochondrial function more appropriately.

Excess blue light at night is a modern problem because the body was not designed for constant artificial brightness. The more we understand light as a biological signal, the more obvious it becomes that darkness matters too.

If we want better sleep, better blood sugar, and better metabolic health, we need to be more careful about the light we expose ourselves to after sunset.

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References

1. Sarode, Bhagyesh R., et al. “Light Control of Insulin Release and Blood Glucose Using an Injectable Photoactivated Depot.” Molecular Pharmacology 13, no. 11, November 7, 2016, 3835-3841. https://doi.org/10.1021/acs.molpharmaceut.6b00633

   Paul, Marla. “Exposure to Bright Light May Alter Blood Sugar.” Futurity, May 19, 2016. https://www.futurity.org/bright-light-metabolism-1166262-2/

2. Rybnikova, Nataliya A., A. Haim, and Boris A. Portnov. “Does Artificial Light-at-Night Exposure Contribute to the Worldwide Obesity Pandemic?” International Journal of Obesity 40, no. 5, May 2016, 815-823. https://doi.org/10.1038/ijo.2015.255

Testosterone Starts with Cholesterol

Here is the basic pathway your body uses to make testosterone:

Cholesterol → Pregnenolone → Androstenedione → Testosterone

That matters because testosterone begins with cholesterol. In fact, every single sex hormone is synthesized from cholesterol. Cholesterol is not just something to fear on a blood test. It is a raw material the body uses to build essential hormones.

This is one reason the conversation around “heart healthy” low-fat, low-cholesterol diets needs more nuance. If the body requires cholesterol to synthesize sex hormones, then aggressively avoiding dietary fat and cholesterol may create problems for hormone production, vitality, and healthy aging.

Testosterone is not produced out of nothing. The body needs the right ingredients. Cholesterol is one of those ingredients.

Research supports this connection. A 1997 study published in the Journal of Applied Physiology looked at testosterone and cortisol in relation to dietary nutrients and resistance exercise. The researchers found that men who consumed more saturated fat, monounsaturated fat, and cholesterol had higher testosterone levels than men who followed a lower-fat diet.¹

This does not mean someone should eat unlimited saturated fat or ignore cardiovascular health. It means that dietary fat and cholesterol should not automatically be treated as enemies. The body uses them for important biological functions, including the production of testosterone and other sex hormones.

The larger point is that hormones are built from nutrients. If the diet is missing key raw materials, the body may struggle to produce hormones at optimal levels. A low-fat, low-cholesterol diet may sound healthy on the surface, but if it compromises the body’s ability to make sex hormones, then it may not support vitality as well as people assume.

Cholesterol has been overly simplified in modern health conversations. It is often discussed only in relation to heart disease risk, while its role in hormone production, cell membranes, brain function, and vitamin D synthesis gets less attention.

That narrow view can lead people to avoid foods their body may actually need.

A better approach is to think about quality, context, and balance. The body needs enough dietary fat to support hormone production, cellular health, and metabolic function. This includes saturated fat, monounsaturated fat, and cholesterol from nutrient-dense foods.

Testosterone starts with cholesterol. That does not make cholesterol good in every context, but it does make it necessary.

And necessary nutrients should not be feared. They should be understood.

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Reference

1. Volek, Jeff S., et al. “Testosterone and Cortisol in Relationship to Dietary Nutrients and Resistance Exercise.” Journal of Applied Physiology 82, no. 1, 1997, 49-54. https://doi.org/10.1152/jappl.1997.82.1.49

Vitamin D and Testosterone: Why Sunlight Still Matters

One of the many problems with the Western diet is that it often lacks key micronutrients the body needs to create hormones. One of the most important is vitamin D.

Vitamin D is essential for testosterone production, and this matters because many people are now deficient in vitamin D. A major reason for this is our overavoidance of UV light. Sunlight is one of the primary ways the body produces vitamin D, but many people have been taught to avoid the sun as much as possible.

That avoidance may come with a cost.

Low vitamin D status is likely one factor involved in declining testosterone levels. Testosterone is not only important for male reproductive health. It also plays a role in muscle mass, strength, energy, mood, libido, motivation, and overall vitality.

A study published in 2010 looked at the vitamin D and testosterone levels of more than two thousand men over the course of a full year. The results showed that men with healthy vitamin D levels had more testosterone and lower levels of sex hormone binding globulin, commonly known as SHBG, than men who were vitamin D deficient.¹

SHBG matters because it binds to hormones, including testosterone, making them less available for the body’s cells to use. If SHBG is elevated, free or bioavailable testosterone may be lower, even when total testosterone does not tell the full story.

In simple terms, vitamin D status may influence both how much testosterone the body produces and how much of that testosterone remains available for use.

This is important because hormone health is often discussed as if it only depends on age, genetics, or medication. But hormones are built from and regulated by the body’s environment. Nutrient status matters. Sunlight matters. Lifestyle matters.

The body cannot produce hormones properly when it is missing the raw materials and signals those systems depend on.

Vitamin D is one of those signals.

The point is not to worship the sun or ignore the risks of burning. Too much UV exposure, especially repeated sunburn, can damage the skin. But avoiding sunlight entirely creates its own problems. The body evolved with regular exposure to natural light, and vitamin D production is one of the clearest examples of why that exposure matters.

A healthier approach is not total avoidance. It is intelligent exposure.

Get sunlight in a way that respects your skin type, season, location, and tolerance. Avoid burning. Use shade, clothing, and protection when needed. But do not forget that sunlight is part of human biology, and vitamin D is part of hormonal health.

If testosterone, energy, strength, and vitality matter, then vitamin D status should not be ignored.

Sometimes supporting hormones begins with the basics: better food, better sleep, strength training, and enough sunlight for the body to make what it needs.

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Reference

1. Wehr, E., et al. “Association of Vitamin D Status with Serum Androgen Levels in Men.” Clinical Endocrinology 73, no. 2, August 2010, 243-248. https://doi.org/10.1111/j.1365-2265.2009.03777.x

How the Body Uses Carbs, Fat, and Protein for Energy

The body needs a continuous supply of glucose to fuel energy metabolism. To keep blood glucose stable, the body works to maintain tight glucose homeostasis within a narrow range, roughly 70 to 90 mg/dl.

It does this in more than one way. The body can convert digested carbohydrates into cellular energy, or it can synthesize glucose in the liver from fatty acids and amino acids through a process called gluconeogenesis. These systems complement one another and provide backup in case one raw nutrient, such as carbohydrates, fats, or protein, is temporarily unavailable.

While fasting and at relative rest, a 155-pound, or 70-kilogram, person requires approximately 200 grams, or about 7 ounces, of glucose over a 24-hour period. The formula used to calculate this demand is 2 mg of glucose per kilogram of body weight per minute.

That 200-gram number is approximate. The actual amount changes depending on the person, body temperature, outside temperature, physical activity, intellectual activity, and other factors. “Additional” activity means anything above and beyond the body’s regular baseline functions, such as heart function, breathing, walking, vision, hearing, and thought.

Any additional activity increases energy needs. This is why both physical and intellectual exertion can increase the body’s energy demand and contribute to weight loss when energy intake is controlled.

Beyond the glucose needed for energy metabolism, the body also needs a continuous supply of fatty acids and amino acids. These are used to build new cells and synthesize hormones, enzymes, vitamins, and other critical substances. These are sometimes called plastic, organic, or replacement needs because they help rebuild or replace dead cells and substances lost through feces, urine, perspiration, and exhaled air.

In simple terms, the body does not need calories only for energy. It also needs raw materials for repair, replacement, and maintenance.

If you consume more than the approximate 200 grams of glucose needed daily, the body can convert the excess into body fat. That is one way fat gain happens.

The rate of conversion is approximately 1 gram of fat for every 3 grams of glucose. This comes from the difference between 9 calories per gram of fat and 4 calories per gram of carbohydrate, with additional allowance for the energy required for consumption, digestion, and conversion.

If you consume less than 200 grams of glucose, the body compensates for the shortage by using fat at a rate of about 1 gram of fat for every 2 grams of glucose. That is one way fat loss happens.

Dr. Atkins incorrectly referred to this process as ketosis because ketones are intermediary products of the biochemical reactions involved in converting fatty acids into cellular energy. The more accurate name for the breakdown of fat is lipolysis.

Before the body converts stored body fat into usable energy, it will use fatty acids derived from food. This means that if dietary fat intake is too high, the body will use fat from the diet before turning to its own fat stores.

According to this framework, consuming above 75 grams of dietary fat can stop the loss of body fat because the body must first dispose of the fat coming from food.

If you consume less than 75 grams of fat, the body will draw from its own fat stores to produce enzymes, hormones, vitamins, cell membranes, and other essential substances. That is another way fat loss occurs.

If you consume more than 75 grams of fat, the excess can be stored under the skin as body fat. That is another way fat gain occurs.

Protein works differently.

If you consume less than 53 grams of protein, the body will break down muscle tissue into amino acids needed for building cells, neurotransmitters, hormones, digestive enzymes, and other essential structures and substances. This process is called muscle wasting.

You can lose weight this way, but it is not desirable weight loss because it is not primarily a loss of body fat. Losing muscle tissue weakens the body, lowers functional capacity, and can negatively affect metabolism.

If you consume more than 53 grams of protein, the body can use the excess amino acids to support muscle tissue. The stronger the muscles, the more protein they can use. In this case, weight gain can occur, but that weight is not from fat. It is desirable weight because it reflects the building or maintenance of lean tissue.

However, if someone does not have strong muscles or does not provide the body with a reason to build muscle, excess protein may not be used for muscle tissue. Instead, some of that excess can be converted into glucose. If the glucose exceeds the body’s energy needs, it can then be converted into body fat.

That is how body fat can be gained from overeating protein.

The larger point is that the body is always trying to solve three problems at once. It needs energy, it needs stable blood glucose, and it needs raw materials for repair and replacement.

Carbohydrates, fats, and proteins all contribute to these needs in different ways. Glucose provides immediate energy. Fat provides stored energy and structural material. Protein provides amino acids for tissue repair, hormones, enzymes, neurotransmitters, and muscle maintenance.

Fat gain and fat loss are not random. They are the result of how the body handles incoming nutrients relative to its current energy needs, replacement needs, and storage demands.

When glucose intake exceeds demand, excess can be stored as fat. When glucose intake is below demand, the body can use fat to compensate. When dietary fat intake is too high, the body may use incoming fat before stored fat. When protein is too low, muscle tissue may be broken down. When protein is adequate and muscles have a reason to use it, protein supports lean tissue. When protein is excessive and not used for muscle, some of it may be converted into glucose and eventually stored as fat.

This is why body composition is not only about calories. It is about how the body uses each nutrient, what it needs at the time, and whether the diet supports energy, repair, and the maintenance of lean tissue.

Happiness Is More Productive Than Pressure

Most people think success creates happiness.

The assumption is simple: once you become more productive, make more money, reach the goal, earn the promotion, build the business, or finally become the person you said you wanted to become, then you will be happy.

But the research suggests the relationship may work in the other direction.

Happy people tend to be more successful than people who are less happy. That may sound like an exaggeration, but it is not. Research discussed by Shawn Achor in Harvard Business Review found that happy people, on average, have 31% higher productivity than their less happy peers. Their sales are 37% higher, and their creativity is three times as high.

That matters because it challenges the way many people approach achievement. They assume happiness is the reward waiting at the end of success. But happiness may actually be one of the conditions that helps create success in the first place.

This does not mean people should ignore discipline, effort, skill, or responsibility. Happiness is not a replacement for competence. It is not a shortcut around hard work. But it does seem to change the way people think, perform, relate, and solve problems.

When someone is happier, their brain is likely operating from a better internal state. They are not wasting as much energy on stress, resentment, fear, or constant dissatisfaction. They are more open, more creative, more resilient, and more capable of seeing possibilities. That improved state can influence how they work, how they communicate, how they sell, how they lead, and how they respond to problems.

Sonja Lyubomirsky, Laura King, and Ed Diener explored this idea in their paper, “The Benefits of Frequent Positive Affect: Does Happiness Lead to Success?” Their research supports the idea that happiness is not merely the result of successful outcomes. Positive affect may help produce the behaviors and conditions that make success more likely.

That distinction is important.

If happiness only comes after success, then people are forced to live in a constant state of postponement. They tell themselves they will feel good once they get somewhere else. Once they reach a certain number. Once they become more accomplished. Once the external world finally gives them permission to relax.

But if happiness helps create success, then learning how to cultivate a better internal state becomes more than a luxury. It becomes part of performance.

This does not mean pretending everything is fine. It does not mean forcing positivity or ignoring pain, stress, grief, frustration, or responsibility. Real happiness is not denial. It is a healthier relationship with life. It is the ability to experience meaning, gratitude, connection, progress, and emotional steadiness while still engaging with difficulty.

Pressure may push people for a while, but it often comes at a cost. Constant dissatisfaction can create urgency, but it can also narrow thinking, reduce creativity, increase stress, and make success feel like survival. Happiness, on the other hand, seems to broaden what people can access within themselves.

A happier person may still work hard, but they are not only being driven by what is missing. They are also being supported by energy, clarity, connection, and a better emotional baseline.

That may be why happiness is linked to higher productivity, better sales, and greater creativity. People perform better when their internal environment supports performance.

The point is not to chase happiness as another achievement. The point is to stop treating happiness as something that must be earned only after everything else is accomplished.

Happiness is not the opposite of ambition. It may be one of the things that makes ambition sustainable.

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References

Achor, Shawn. “Positive Intelligence.” Harvard Business Review, January-February 2012. https://hbr.org/2012/01/positive-intelligence

Lyubomirsky, Sonja, Laura King, and Ed Diener. “The Benefits of Frequent Positive Affect: Does Happiness Lead to Success?” Psychological Bulletin 131, no. 6, November 2005, 803-855. https://www.apa.org/pubs/journals/releases/bul-1316803.pdf

The Gut-Skin Connection Behind Sun Sensitivity

Melanoma rates have increased alongside the increased use of sunscreen. That does not prove sunscreen causes melanoma, but the correlation raises an uncomfortable question. If sunscreen is supposed to protect us from the harmful effects of the sun’s rays, why have melanoma rates continued to rise while sunscreen use has also increased?

One proposed explanation is that the problem may not be sunlight alone. The connection may involve the way modern chemical exposure interferes with the body’s natural ability to protect itself from the sun.

One chemical often discussed in this context is glyphosate, the herbicide used in Roundup. The concern is that glyphosate may disrupt the skin’s natural sun-protection mechanisms by affecting the gut microbiome.

Gut microbes normally help produce tryptophan and tyrosine, two amino acids that serve as precursors to melanin. Melanin is the dark compound found in tanned or naturally darker skin. Its role is not cosmetic. Melanin helps absorb ultraviolet light and protect the skin from the damage that excessive UV exposure can cause.

In a healthy system, the body has built-in protective mechanisms that help it respond to sunlight. The skin darkens, melanin increases, and the body becomes better equipped to tolerate sun exposure.

But if food is exposed to glyphosate, the theory is that glyphosate may negatively affect gut microbes. When those microbes are disrupted, they may not produce enough of the amino acids involved in melanin production. As a result, the body’s natural mechanisms for sun protection may become less effective.

From this perspective, dangerous sunburns and possibly even melanoma may not be caused by exposure to the sun alone. They may also reflect a deeper issue involving chemical exposure, microbiome disruption, impaired amino acid production, and weakened melanin formation.

That does not mean sunlight is harmless. Too much sun exposure, especially when the skin burns, can damage the skin. But it does suggest that blaming the sun by itself may be an incomplete explanation.

The body is designed to interact with sunlight. Sunlight helps regulate circadian rhythm, vitamin D production, mood, hormones, and many other biological processes. The issue may be that modern lifestyles and chemical exposures have changed the body’s ability to handle sunlight appropriately.

If glyphosate interferes with the gut bacteria needed to support melanin production, then the problem is not simply that people are spending time in the sun. The problem may be that people are entering the sun with weaker biological defenses than they should have.

Diet may matter here as well.

The body also needs plenty of polyphenols, compounds found in brightly colored plants, to support healthy skin and melanin production. Melanin is made out of cross-linked polyphenols, which means the quality of the diet can influence how well the skin builds its natural protective pigments.

This gives us a broader way to think about sunburn.

Sunburn is not only a problem of too much sun. It may also be a problem of too little internal resilience. If the gut microbiome is compromised, if amino acid production is impaired, if polyphenol intake is low, and if chemical exposure is high, then the skin may be less prepared to respond to sunlight in the way it was designed to.

That does not mean sunscreen has no place. It does mean sunscreen should not be treated as the entire solution.

A better approach to sun protection would include both external and internal factors. External protection may include shade, clothing, gradual exposure, and sunscreen when appropriate. Internal protection would include supporting the gut microbiome, reducing exposure to chemicals that may harm it, eating a nutrient-rich diet, and consuming foods rich in polyphenols.

The larger point is that sunlight may not be the villain it is often made out to be. The body’s relationship with the sun depends on context. A healthy, well-nourished body with a strong microbiome may respond to sunlight differently than a chemically burdened, nutrient-depleted body with compromised skin defenses.

Glyphosate may be one piece of that larger conversation.

If chemical exposure disrupts the gut microbes that help create the building blocks for melanin, then modern sun sensitivity may be less about the sun itself and more about the loss of the biological systems that help us interact with the sun safely.

The question is not only, “How do we block the sun?”

The better question may be, “Why are our bodies becoming less able to handle it?”

Viruses Are Just Information

Imagine a situation where the human community is confronted with a new toxin.

This toxin can only be neutralized by an enzyme that human beings do not usually make. But one member of the community has a randomly generated mutation that allows her, and only her, to make the toxin-neutralizing enzyme. She does well, while others become sick and some die because this mutation gives her an adaptive advantage.

According to the theory of genetic mutation and natural selection, her genes would slowly spread throughout the population. Over time, the adaptive mutation would become more common because it helps people survive.

But what happens if she is a sixty-year-old postmenopausal woman? What if she is a man who does not have children? In that case, the helpful gene dies out.

If we are lucky, maybe the carrier of the gene is a thirty-year-old man about to get married. He and his wife have six children, and three of them carry the autosomal dominant mutation. One of those three dies in a car crash. Another becomes sterile. The third passes the adaptive gene on to her two children.

In ten thousand years, that adaptive gene may have spread throughout the population through natural selection. Unfortunately, by then, the toxin has either killed everyone off or is long gone, making the mutation useless.

This creates an important question.

Can the theory of natural selection following random mutations fully explain how humans and animals adapt to new situations quickly enough for those mutations to be useful?

If adaptation only happens through random mutation and reproduction across generations, the process may be too slow to explain real-time biological response to rapidly changing environments. Life often has to respond faster than that.

So how do organisms adapt in real time?

One proposed way to think about this is through exosomes. When cells are threatened, they can produce exosomes containing DNA and RNA. These tiny packages of genetic material are involved in communication between cells. They carry information from one part of the body to another and may help coordinate biological responses to changing conditions.

From this perspective, what we call “viruses” may be understood differently. Rather than thinking of viruses only as hostile invaders, this view suggests they may function as physical-resonance forms of genetic material that code for changes happening in the environment.

In that interpretation, viruses are not simply enemies. They are carriers of biological information.

They may represent a system of real-time genetic adaptation. Instead of waiting thousands of years for a useful mutation to spread through reproduction, genetic information could move more quickly between cells, organisms, or populations. This would create a much faster way for life to respond to environmental pressure.

That is the larger idea behind the claim that viruses are information.

Unlike bacteria, which can be grown in a petri dish and are clearly living organisms, viruses are not alive in the same way. They do not independently metabolize. They do not reproduce on their own. They are pieces of genetic material packaged in a protein coat, dependent on cells to replicate.

In simple terms, viruses can be thought of as packets of information.

They carry instructions. They interact with the genome. They may influence which biological switches are turned on or off. In this view, viruses are not merely agents of disease. They are genetic messengers that may participate in how organisms respond to environmental change.

This way of thinking also changes how we interpret sickness.

If someone becomes overtly sick, one possibility is that the body could not handle the “download” of information. Another possibility is that the new biological instructions did not match the person’s internal health, lifestyle, or external environment. In other words, the issue may not only be exposure. It may also be the condition of the terrain receiving the signal.

This does not mean illness is imaginary. It does not mean viruses are harmless. It means there may be more to the story than the idea that viruses are only hostile forces trying to attack us.

The conventional model often treats viruses as dangerous invaders that must be fought. But if viruses also function as carriers of environmental information, then a total war on viruses may reflect a misunderstanding of their role in nature.

A virus may not be alive in the way bacteria are alive. It may be closer to information. A signal. A message. A set of instructions.

The role of viruses in nature, from this perspective, is to help recode genetic material in response to changes happening in the environment. They may provide a mechanism for real-time genetic adaptation.

That is a very different way to understand biology.

Instead of seeing life as a battlefield where organisms defend themselves against endless microbial enemies, this view sees life as a communication system. Cells communicate. Organisms communicate. Genetic information moves. The environment changes, and biology responds.

Viruses may be part of that communication.

The question is whether we are willing to look at them through a wider lens.

If we assume viruses are only hostile and dangerous, then our only response is fear, suppression, and war. But if viruses are also information, then we may need to rethink the relationship between illness, adaptation, genetic expression, environment, and evolution.

Maybe the body is not simply being attacked.

Maybe it is receiving information.

Maybe sickness is sometimes the cost of a system trying to adapt to instructions it is not currently healthy enough to process smoothly.

This idea may sound strange because it challenges the standard story. But the standard story does not always explain how quickly life adapts, how genetic information moves, or why the same exposure can affect different people in different ways.

Viruses may not be the enemy in the way we have been taught to imagine them.

They may be part of the language life uses to communicate with itself.

Gene Expression Is Based on Context

The news continues to report that genes are the cause of this or that. One gene is linked to alcoholism. Another gene is linked to obesity. Another gene is linked to depression. Our first instinct is to label the gene as “good” or “bad” based on what it is said to produce.

If a gene is associated with something negative, we assume the gene itself must be negative. It becomes a “bad” gene. It becomes something to fear, avoid, or blame.

Psychologists have traditionally described this through something called the diathesis-stress model. The basic idea is that if you have a genetic vulnerability and you encounter enough stress in life, you may be more likely to develop a disorder such as depression, anxiety, addiction, or some other unwanted outcome.

In that model, the gene is treated like a risk factor waiting to be activated by stress. If you have the “bad” gene and life becomes difficult enough, the assumption is that the gene may push you toward a negative outcome.

The problem is that this way of thinking may be incomplete.

Recent discoveries in genetics have challenged the simple good gene versus bad gene model. More and more, the evidence points toward environmental context. The same gene that may create problems in one environment may produce advantages in another.

Psychologists call this the differential susceptibility hypothesis.

The idea is that some genes do not simply make someone more vulnerable to bad outcomes. Instead, they may make someone more sensitive to their environment. In a poor environment, that sensitivity may lead to worse outcomes. In a supportive environment, that same sensitivity may lead to better outcomes.

This changes the whole conversation.

The gene itself is not automatically good or bad. The outcome depends on the input.

A simple way to think about this is with a knife. The same knife can be used to hurt someone, or it can be used to prepare food. The knife is not inherently good or bad. Its value depends on how it is used, who is using it, and the context it is placed in.

Genes may work in a similar way.

One example is the DRD4 gene. Most people have the standard version of this gene, but some people have a variant called DRD4-7R. This 7R variant has been associated with ADHD, alcoholism, and violence, so it has often been thought of as a “bad” gene.

But the story is not that simple.

In a study by Ariel Knafo, researchers looked at which children would share candy without being asked. The children were only three years old. Interestingly, the children who had the 7R variant were more likely to share than those who did not have the so-called “bad” variant.

That raises an important question: why were the children with the “bad” gene more inclined to help, even when nobody asked them to?

The answer is that 7R is not inherently bad. Like the knife, it depends on context.

Children with the 7R variant who were raised in rough environments, especially environments marked by abuse or neglect, were more likely to develop negative outcomes such as alcoholism or bullying behavior. But children with the 7R variant who received good parenting were seen as kinder than children who had the standard DRD4 gene.

That is a radically different way to understand genetics.

The same genetic variant that may be linked to negative outcomes in one environment may be linked to positive outcomes in another. The gene is not destiny. It is a sensitivity. It is a responsiveness. It is a potential that can express itself differently depending on the environment around it.

This is why context matters so much.

The body does not express genes in a vacuum. Genes respond to signals. They respond to stress, nutrition, parenting, relationships, sleep, movement, trauma, safety, toxins, light, and the broader environment. The question is not only, “What genes do you have?” The better question is, “What environment are those genes being asked to respond to?”

That distinction matters because it gives us a more useful way to think about health, behavior, and human development.

If we believe genes are fixed causes, then people become prisoners of their biology. A person with a gene associated with alcoholism, depression, ADHD, obesity, or violence may begin to believe their future is already written. But if gene expression depends on context, then the environment becomes part of the story.

Lifestyle matters. Parenting matters. Stress matters. Relationships matter. Inputs matter.

This does not mean genetics are irrelevant. It means genetics are not the whole explanation. Genes may create tendencies, sensitivities, or probabilities, but they do not operate separately from the conditions of a person’s life.

The good gene versus bad gene model is too simple. It misses the deeper reality that biology is responsive. A gene that looks like a liability in one environment may become an advantage in another.

That should change the way we talk about human potential.

Instead of asking whether a gene is good or bad, we should ask what kind of environment brings out its worst expression and what kind of environment brings out its best expression.

That is where the real conversation begins.

Gene expression is based on context.

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Source

Barker, Eric. Barking Up the Wrong Tree.

Time Isn’t Linear

In July 2000, Israeli doctor Leonard Leibovici conducted a double-blind, randomized controlled trial involving 3,393 hospital patients. The patients were divided into a control group and an “intercession” group. The purpose of the experiment was to see whether prayer could have an effect on their condition.

Prayer experiments are often used as examples of mind affecting matter at a distance. But this particular study is especially interesting because the story is not quite what it appears to be at first.

Leibovici selected patients who had suffered sepsis, an infection, while hospitalized. He randomly designated half of the patients to have prayers said for them, while the other half were not prayed for. He then compared the results across three categories: how long fever lasted, length of hospital stay, and how many patients died as a result of the infection.

The prayed-for group benefited from an earlier decrease in fever and a shorter hospitalization time. The difference in the number of deaths between the prayed-for group and the group that was not prayed for was not statistically significant, although mortality was slightly better in the prayed-for group.

At first, that sounds like a powerful demonstration of the benefits of prayer and the possibility that intention may influence the body through thoughts and feelings. But there is one additional element to this story that makes it even more provocative.

Did it strike you as odd that in July 2000, one hospital would have more than 3,000 cases of infection at once? Was it a very poorly sterilized place, or was some kind of contagion running rampant?

That is where the study becomes strange.

The people praying in 2000 were not praying for patients who were infected in 2000. Unbeknownst to them, they were praying for lists of people who had been hospitalized between 1990 and 1996, four to ten years before the experiment took place. The patients being prayed for had already gone through their illness years earlier.

In other words, the study examined remote, retroactive intercessory prayer.

That means the prayers were said after the medical events had already happened. The prayed-for patients appeared to show measurable differences in outcomes, but those outcomes had taken place years before the intervention was performed.

That is what makes this study so difficult to categorize.

If read literally, it seems to challenge the way we usually think about time, cause, and effect. We normally assume the past is fixed, the present is unfolding, and the future has not happened yet. Cause comes before effect. An action happens, and then something follows from it.

But in this study, the “intervention” happened years after the outcomes being measured.

This does not mean the study proves that time is not linear. It does not prove that prayer can change the past. It does not prove that intention can rewrite medical outcomes across time. A careful reading should avoid turning one provocative study into a final conclusion.

What it does show is that evidence can sometimes raise questions that do not fit neatly into the assumptions we already hold.

That may be the real value of the study. It forces us to sit with something uncomfortable: what if our ordinary model of time is incomplete? What if cause and effect are not always as simple as we assume? What if consciousness, intention, and biological systems are connected in ways that are not yet fully understood?

The study was published in the British Medical Journal in 2001 under the title “Effects of Remote, Retroactive Intercessory Prayer on Outcomes in Patients with Bloodstream Infection: Randomised Controlled Trial.” Its conclusion stated that remote, retroactive intercessory prayer was associated with shorter hospital stay and shorter duration of fever in patients with bloodstream infection.

Again, “associated with” matters. This should not be treated as proof that a later prayer caused an earlier recovery. But it is still a fascinating example of how certain findings can disturb the clean categories we use to understand reality.

Most of us experience time as linear. We remember the past, live in the present, and move toward the future. That experience is practical and necessary. It allows us to organize life, make decisions, and understand consequences.

But studies like this invite a different kind of reflection. They do not require us to abandon reason. They ask us to stay open to the possibility that reality may be stranger than the simplified model we use to navigate it.

Maybe time is linear in the way we experience it.

Maybe it is not linear in every possible sense.

Maybe the deeper point is that our perception of time may not be the same as the full nature of time.

That is why this story matters. It does not need to be embellished. It is already strange enough on its own. A randomized controlled trial was conducted in 2000 using patients from 1990 to 1996, and the group prayed for years later showed shorter fever duration and hospital stays in the original records.

Whether that points to prayer, probability, study design, consciousness, or something we do not yet understand, it challenges the assumption that all causation must move in the direction we expect.

Sometimes the most important studies are not the ones that give us clean answers. They are the ones that force us to ask better questions.

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Reference

Leibovici, Leonard. “Effects of Remote, Retroactive Intercessory Prayer on Outcomes in Patients with Bloodstream Infection: Randomised Controlled Trial.” BMJ 323, no. 7327, December 22, 2001, 1450–1451. https://doi.org/10.1136/bmj.323.7327.1450

The Power of Placebo

The placebo effect is usually discussed as if it is imaginary, fake, or secondary to “real” medicine. But that understanding may be too dismissive. The placebo effect does not mean nothing happened. It means the body responded to expectation, belief, context, and perceived meaning.

An interesting example comes from research conducted in the cardiac ward of a major American hospital with patients suffering from angina.

Angina is a condition where the arteries supplying the heart become restricted, producing acute chest pain. Digitalis, traditionally derived from the foxglove plant, has been used to help relieve the acute symptoms of an angina attack. Once administered, it generally brings fast relief.

In this experiment, patients who suffered from an acute angina attack were split into two groups. Fifty percent were given digitalis, while the other fifty percent were given a placebo. The second group received only sugar tablets, yet a significantly high proportion of them responded favorably and their symptoms subsided.

That finding alone is interesting because it shows that the body can respond powerfully to belief and expectation. The patients were not receiving the active drug, but many still experienced relief.

The more interesting part of the experiment was what happened with the doctors.

Half of the doctors who prescribed the placebo knew they were giving a placebo. The other half believed they were giving their patients the real drug. Surprisingly, the patients who received a placebo from doctors who thought they were prescribing the real medication responded much better than the patients who received a placebo from doctors who knew they were prescribing a sugar tablet.

That detail matters.

It suggests that the placebo effect is not only about the patient’s belief. The doctor’s confidence may also influence the patient’s response. In other words, healing is not shaped only by the substance being given. It may also be shaped by the interaction, the expectation, the tone, the certainty, and the meaning created around the treatment.

This does not mean medicine is fake. It does not mean drugs do nothing. Digitalis has real pharmacological effects. But it does suggest that the body is more responsive to context than many people realize.

The belief of the patient matters. The confidence of the doctor matters. The relationship between the two may matter as well.

That should make us think more carefully about healing. If the body can respond differently depending on belief, expectation, and the confidence of the person providing care, then the clinical encounter itself is not neutral. The way something is communicated can become part of the treatment.

A dismissive doctor may create one biological response. A confident doctor may create another. A patient who feels reassured may respond differently than a patient who feels uncertain or afraid.

This is the power of placebo.

It is not proof that symptoms are imagined. It is proof that the body and mind are not separate. What a person believes, expects, and feels can influence how the body responds. The brain, nervous system, immune system, hormones, pain perception, and cardiovascular system are all connected. The meaning attached to an intervention may change the way those systems behave.

The placebo effect should not be treated as an embarrassing flaw in medicine. It should be treated as evidence that healing involves more than chemistry alone.

The body responds to information. Sometimes that information comes in the form of a drug. Sometimes it comes through confidence, trust, expectation, and belief.

That does not make placebo less real.

It may make it one of the clearest examples of how powerful the body can be when it believes healing is possible.

K2 Deficiency Might Be Written All Over Your Face

The skin is often treated as a cosmetic issue, but it may reveal more about internal health than we realize. Wrinkles, skin firmness, and tissue quality may not only reflect age or sun exposure. In some cases, they may also reflect what is happening in the bones, kidneys, and vitamin K2-dependent systems of the body.

One example comes from research on postmenopausal women. Specifically, the severity of a postmenopausal woman’s facial wrinkles appears to predict her risk of osteoporosis. Women with more extensive facial wrinkles were found to be much more likely than their peers to have low bone mass, while women with firmer skin tended to have denser bones. This relationship appeared regardless of age or body weight.¹

That matters because osteoporosis is usually thought of as a bone issue, while wrinkles are usually thought of as a skin issue. But the body does not separate itself into isolated cosmetic and structural categories. Skin quality and bone quality may be connected through deeper biological processes, including collagen, mineral metabolism, and vitamin K-dependent proteins.

A similar connection appears in research on kidney function. Korean research published in Nephrology in 2008 found that increased facial wrinkling was associated with reduced kidney filtration rate, which is a measure of kidney function. This association was found independent of age and sex.²

That finding becomes even more interesting when paired with American research published the following year. In 2009, researchers found that decreased kidney filtration predicted an increase in inactive matrix Gla protein, often abbreviated as MGP.³

MGP is a vitamin K-dependent protein. When vitamin K2 status is insufficient, MGP remains inactive. That matters because active MGP helps regulate calcium placement in the body. In simple terms, vitamin K2 helps activate proteins that guide calcium into the right places and away from places where it does not belong.

This is where the skin connection becomes more meaningful. If increased facial wrinkling is associated with reduced kidney filtration, and reduced kidney filtration is associated with higher levels of inactive MGP, then facial wrinkles may point toward something deeper than skin aging alone.

They may reflect a broader issue involving vitamin K2-dependent biology.

This does not mean every wrinkle is a sign of vitamin K2 deficiency. Aging, sun exposure, smoking, stress, hydration, genetics, nutrition, and hormone changes all influence the skin. But the research does suggest that facial wrinkling may be connected to internal health markers in ways we often overlook.

When it comes to skin, a K2 deficiency might be written all over your face.

The larger point is that the body gives clues. Skin is visible, which makes it easy to dismiss as superficial. But visible signs can sometimes reflect invisible processes. The skin, bones, kidneys, blood vessels, and mineral-regulating proteins are all part of the same biological system.

Vitamin K2 sits at an important intersection in that system. It helps activate proteins involved in bone mineralization and calcium regulation, including osteocalcin and MGP. When these proteins remain inactive, the body may struggle to manage calcium properly.

That is why wrinkles, bone density, kidney function, and inactive MGP may belong in the same conversation. They may seem unrelated at first, but they all point toward the same idea: external signs can reflect internal function.

A face does not tell the whole story, but it may give hints. Skin quality may be one of the visible ways the body reveals changes happening beneath the surface.

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References

1. Pal, L., Kidwai, N., Glockenberg, K., et al. “Skin Wrinkling and Rigidity Are Predictive of Bone Mineral Density in Early Postmenopausal Women.” Endocrine Reviews 32, no. 03 Meeting Abstracts, 2011, 3–126.

2. Park, B. H., Lee, S., Park, J. W., et al. “Facial Wrinkles as a Predictor of Decreased Renal Function.” Nephrology 13, no. 6, 2008, 522–527.

3. Parker, B. D., et al. “Association of Kidney Function and Uncarboxylated Matrix Gla Protein: Data from the Heart and Soul Study.” Nephrology Dialysis Transplantation 24, no. 7, 2009, 2095–2101. https://doi.org/10.1093/ndt/gfp024

Our Bones Impact Insulin Sensitivity

Most people think of the skeleton as structure. Bones hold us upright, protect organs, give muscles leverage, and allow us to move through the world. In that sense, the skeleton is usually imagined as a kind of living scaffolding.

But research has shown that the skeleton may be far more active than that.

In 2007, groundbreaking research published in Cell revealed that the skeleton, through the vitamin K2-dependent protein osteocalcin, has a significant impact on the body’s production of insulin and sensitivity to insulin. This finding changed the way scientists understood bone. Instead of seeing the skeleton as inert support tissue, the research suggested that bone also functions as a dynamic endocrine organ.

That is a major shift.

An endocrine organ produces signaling molecules that influence other systems in the body. We usually think of endocrine function in relation to glands such as the thyroid, pancreas, adrenals, or reproductive organs. But this research suggested that bone also communicates with metabolism.

The key player is osteocalcin, a protein produced within bone. Osteocalcin is vitamin K2-dependent, meaning vitamin K2 plays an important role in its function. According to the researchers, osteocalcin has the capacity to improve glucose tolerance and influence insulin production and insulin sensitivity.

That matters because insulin resistance is one of the defining features of type 2 diabetes. When the body becomes resistant to insulin, glucose regulation becomes impaired. Blood sugar stays elevated more easily, the pancreas has to work harder, and metabolic dysfunction begins to develop over time.

If bone-derived osteocalcin helps regulate insulin production and sensitivity, then bone health is not only about fractures, posture, or density. It is also connected to metabolic health.

This makes vitamin K2 important in a way many people do not fully appreciate. Vitamin K2 is often discussed in relation to calcium metabolism and bone health, but its relationship with osteocalcin connects it to a much larger conversation. If osteocalcin influences glucose tolerance and insulin sensitivity, then supporting vitamin K2 status may be relevant to the prevention of insulin-resistant diabetes.

The larger point is that the body is not a collection of disconnected parts. Bone affects metabolism. Nutrients affect hormones. Hormones affect blood sugar. The skeleton communicates with the pancreas, energy regulation, and glucose handling.

This is why reductionist thinking often fails in health. When we think of bones only as structure, we miss their role in signaling. When we think of insulin resistance only as a blood sugar problem, we may miss the other tissues and nutrients involved in metabolic regulation.

The 2007 discovery made a strong case that the skeleton should be understood as part of the endocrine system. Bone is not just something the body carries around. It is metabolically active tissue that participates in whole-body regulation.

Our bones do more than hold us up. They help communicate with the systems that determine how well we produce insulin, respond to insulin, and manage glucose.

That means bone health and metabolic health are more connected than most people realize.

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Reference

Lee, N. K., Sowa, H., Hinoi, E., et al. “Endocrine Regulation of Energy Metabolism by the Skeleton.” Cell 130, no. 3, 2007, 456–469. https://doi.org/10.1016/j.cell.2007.05.047

Snacking Is Stupid

Prior to 1977, Americans did not just eat more dietary fat and fewer refined grains. They also ate less often.

That part of the nutrition conversation does not get nearly enough attention. Most people focus on what changed in the diet, but eating frequency changed too. There were no official recommendations telling people to abandon structured meals and start eating all day, but eating patterns changed anyway.

That shift may have contributed to the obesity crisis.

The National Health and Nutrition Examination Survey, or NHANES, found that in 1977 most people ate three times per day: breakfast, lunch, and dinner. Eating was organized around meals, not constant grazing. If a child wanted an after-school snack, the typical answer from mom was, “No, you’ll ruin your dinner.” If they wanted a bedtime snack, the answer was usually no again.

Snacking was considered neither necessary nor especially healthy. A snack was a treat. It happened occasionally, not automatically.

Now, the message has changed. We are often told that eating more frequently helps with weight loss. The idea is that more frequent meals or snacks somehow “stoke the metabolism,” control hunger, or make fat loss easier. The problem is that this assumption has been repeated far more than it has been proven.

The scientific support for eating more frequently as a weight-loss strategy is weak. Its respectability seems to come mostly from repetition. At first glance, the idea sounds pretty stupid. And it sounds stupid because, in most cases, it is.

Snacking creates more opportunities to eat. More opportunities to eat can easily become more opportunities to overeat. This is especially true in a modern food environment where snacks are rarely just small portions of whole foods. They are usually highly palatable, easy to consume, calorie-dense, and designed to be eaten quickly.

The issue is not that a snack can never have a place. The issue is that snacking has been normalized as if the human body requires constant feeding to function well. Historically, that was not how most people ate. Most people ate meals, then stopped eating until the next meal.

That structure matters.

When eating is built around breakfast, lunch, and dinner, hunger and satiety have a clearer rhythm. You eat, you digest, you become hungry again, and you eat the next meal. When eating becomes constant, that rhythm gets blurred. Food becomes less tied to hunger and more tied to habit, boredom, stress, convenience, availability, or marketing.

That is exactly the question raised by Barry Popkin and Kiyah Duffey in their paper, “Does Hunger and Satiety Drive Eating Anymore?” The title alone points to the problem. Modern eating patterns have shifted toward more eating occasions and less time between those eating occasions.¹

This matters because hunger and satiety should mean something. They are part of the body’s regulatory system. But when food is always available, and when snacks are treated as a normal part of the day, eating can become disconnected from actual physical need.

A person may not be hungry. They may just be used to eating at that time.

They may not need food. They may just be tired, stressed, bored, distracted, or surrounded by snacks.

They may not be supporting their metabolism. They may simply be adding calories they never needed in the first place.

That is why snacking deserves more scrutiny. It is often presented as a helpful habit, but for many people, it may be one of the quiet reasons they struggle to lose weight. A handful of food here, a protein bar there, a few bites after dinner, something sweet before bed, and suddenly the calorie deficit they thought they were creating is gone.

The body does not need to be fed constantly. Most people do not need six meals a day. Most people do not need a snack between every meal. And most people trying to lose weight would probably benefit from fewer eating occasions, not more.

This is especially true when the goal is fat loss.

A simple meal structure creates boundaries. Breakfast, lunch, and dinner give the day a clear rhythm. It becomes easier to know when eating starts and when eating stops. It becomes easier to build meals around protein, whole foods, and adequate nutrition instead of trying to manage constant hunger with random snacks.

Again, this does not mean a snack is always wrong. A hard-training athlete, someone with higher calorie needs, a person with blood sugar issues, or someone who genuinely needs more food within their day may have a reason to include one. But that is different from treating snacking as a universal recommendation.

The problem is not the occasional snack. The problem is the belief that constant eating is necessary, healthy, or automatically helpful for weight loss.

For most people, snacking is not a strategy. It is a leak in the system.

If the goal is better health, better appetite control, and better body composition, the first step may be returning to a simpler structure: eat real meals, make them satisfying, prioritize protein and whole foods, and stop treating every passing urge to eat as a biological emergency.

Snacking became normal. That does not mean it became useful.

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Reference

Popkin, B. M., & Duffey, K. J. “Does Hunger and Satiety Drive Eating Anymore? Increasing Eating Occasions and Decreasing Time Between Eating Occasions in the United States.” American Journal of Clinical Nutrition 91, no. 5, 2010, 1342–1347. https://doi.org/10.3945/ajcn.2009.28962

Just Take a Tylenol

“Just take a Tylenol.”

This might as well be the American mantra. It reflects the perspective many of us have been taught to adopt: that the body is full of annoying symptoms, and the easiest response is to suppress them with drugs.

The main ingredient in Tylenol is acetaminophen, which has been used in the United States for more than 70 years. It is considered a benign over-the-counter medication, used reflexively for aches, pains, and fever, and is widely thought of as safe during pregnancy. About 23 percent of American adults, or roughly 52 million people, use a medicine containing acetaminophen each week. It is the most common drug ingredient in the United States and is found in more than 600 medicines. However, this “harmless” drug has been linked to more than 110,000 injuries and deaths per year.¹

So how can Tylenol, something handed out so casually, be harmful?

One surprising part of the conversation is that researchers still do not fully know exactly how acetaminophen works.² What is known is that the drug reaches the brain, and that matters because acetaminophen can deplete glutathione, an antioxidant that is especially important for brain health.³

Glutathione helps the body balance oxidative damage and inflammation. When a medication affects that system, it should at least make us think more carefully about how casually we use it.

This does not mean acetaminophen has no place. It means the phrase “just take a Tylenol” may be far too casual for a drug that affects important biological systems and is used so frequently.

The same broader concern applies to other common pain relievers, including NSAIDs. NSAIDs are often used for pain and inflammation, but they can injure the small intestine. In one study, 71 percent of chronic NSAID users showed visible small-intestinal damage, compared to 10 percent of nonusers.⁴

Damaged intestines can contribute to intestinal permeability, often called “leaky gut” or gut permeability. This matters because gut permeability has been linked with conditions such as depression, ADHD, and allergies. NSAIDs can induce gut permeability and may also harm the microbiome, the inner ecology of organisms that supports overall wellness.⁵

This is the larger problem with our reflexive approach to pain. We are often taught to see symptoms as inconveniences to silence rather than signals to understand. A headache, ache, pain, or fever may be uncomfortable, but discomfort is not automatically meaningless. It is often information.

When the first response is always suppression, we may miss the opportunity to ask why the symptom appeared in the first place.

That does not mean every headache needs deep investigation. It does not mean pain relievers should never be used. It means we should be more thoughtful about reaching for them automatically, especially when they are used often, casually, or without considering the broader effects they may have on the body.

Once we understand the potential concerns with Tylenol and other NSAIDs, the next question becomes obvious: what can someone use for headaches and other aches and pains?

One natural option worth discussing is turmeric, the yellow root found in curry powder. Turmeric contains curcumin, a compound with anti-inflammatory and pain-relieving properties. It has been used in Ayurvedic and Chinese medicine for centuries as a treatment for pain, digestive disorders, and wound healing.

Several studies have shown beneficial effects of curcumin. Research has found that curcumin may work as well as ibuprofen for pain related to knee osteoarthritis.⁶ Another study comparing ginger, mefenamic acid, and ibuprofen found benefit for pain in women with primary dysmenorrhea.⁷

So the next time you have a headache, it may be worth considering 1 to 2 grams of curcumin, or even a turmeric latte, depending on the situation.

The point is not that natural options are always better or that medications are always bad. The point is that “just take a Tylenol” should not be the only way we think about pain.

Pain is not always the enemy. Sometimes it is a message. The goal should not always be to silence the body as quickly as possible. The goal should be to understand what the body is saying, respond appropriately, and use any intervention, natural or pharmaceutical, with more awareness.

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References

1. T. Christian Miller and Jeff Gerth, “Behind the Numbers: We Explore the Data Behind Figures Showing How Many People Die from Overdosing on Acetaminophen, the Active Ingredient in Tylenol,” ProPublica, September 20, 2013. www.propublica.org/article/tylenol-mcneil-fda-behind-the-numbers

2. Carmen Drahl, “How Does Acetaminophen Work? Researchers Still Aren’t Sure,” Chemical and Engineering News 92, no. 29, July 21, 2014, 31–32. https://cen.acs.org/articles/92/i29/Does-Acetaminophen-Work-Researchers-Still.html

3. John T. Slattery et al., “Dose-Dependent Pharmacokinetics of Acetaminophen: Evidence of Glutathione Depletion in Humans,” Clinical Pharmacology and Therapeutics 41, no. 4, April 1987, 413–418. https://doi.org/10.1038/clpt.1987.50

4. D. Y. Graham et al., “Visible Small-Intestinal Mucosal Injury in Chronic NSAID Users,” Clinical Gastroenterology and Hepatology 3, no. 1, January 2005, 55–59. PMID: 15645405.

5. G. Sigthorsson et al., “Intestinal Permeability and Inflammation in Patients on NSAIDs,” Gut 43, no. 4, October 1998, 506–511. PMID: 9824578.

6. V. Kuptniratsaikul et al., “Efficacy and Safety of Curcuma domestica Extracts in Patients with Knee Osteoarthritis,” Journal of Alternative and Complementary Medicine 15, no. 8, August 2009, 891–897. https://doi.org/10.1089/acm.2008.0186

7. G. Ozgoli et al., “Comparison of Effects of Ginger, Mefenamic Acid, and Ibuprofen on Pain in Women with Primary Dysmenorrhea,” Journal of Alternative and Complementary Medicine 15, no. 2, February 2009, 129–132. https://doi.org/10.1089/acm.2008.0311

Sugar Is Bad for Your Brain

Sugar is usually discussed in the context of weight gain, blood sugar, or diabetes, but its effects go much deeper than that. Sugar also has consequences for the brain, partly because the brain depends heavily on energy metabolism, mitochondrial function, neurotransmitter signaling, and inflammation control.

Scientists have known there is a relationship between sugar and cellular energy production for a long time. In 1927, biochemist Herbert Crabtree discovered that elevated glucose levels could lower mitochondrial function. This matters because mitochondria are responsible for producing the energy our cells rely on to function properly.

When mitochondrial function is impaired, the issue is not only about energy. Mitochondria are involved in cellular health, oxidative stress, inflammation, and the way tissues throughout the body respond to metabolic stress. Since the brain is one of the most energy-demanding organs in the body, anything that negatively affects mitochondrial function has the potential to affect brain health.

Sugar has also been shown to decrease the number of dopamine receptors in the brain. Dopamine is closely tied to motivation, reward, pleasure, drive, and reinforcement. When dopamine signaling is altered, it can affect how the brain responds to food, reward, and repeated exposure to highly palatable foods.

This is one reason sugar can be so difficult for people to moderate. The issue is not only that sugar tastes good. It also interacts with the brain’s reward system in a way that can influence cravings, habits, and the desire to keep consuming more.

While all forms of sugar can become a problem when consumed excessively, fructose appears to be especially concerning. Fructose is found in fruit, high-fructose corn syrup, and agave nectar. The context matters, though. Eating moderate amounts of whole, seasonal fruit is very different from consuming large amounts of fructose through fruit juice, sweetened beverages, processed foods, high-fructose corn syrup, or agave nectar.

Fructose can contribute to oxidative stress and may also feed less beneficial bacteria in the gut, which can promote inflammation. That matters because the gut and brain are not separate systems. Inflammation that begins in the gut can influence the rest of the body, including the brain.

Fructose has also been implicated in damaging mitochondria in skeletal muscle cells, harming the mitochondrial membrane, and impairing cellular respiration and energy metabolism. In simple terms, excessive fructose may interfere with the body’s ability to produce energy efficiently at the cellular level.

The brain will usually tolerate moderate amounts of whole fruit, especially when that fruit is seasonal and eaten in its natural form. Whole fruit comes packaged with water, fiber, micronutrients, and other compounds that slow down absorption and make overconsumption less likely.

Fruit juice is different. High-fructose corn syrup is different. Agave nectar is different. These sources make it much easier to consume large amounts of fructose without the same natural limits that come with eating whole fruit.

For that reason, a practical approach is to avoid excessive fructose intake, completely stay away from fruit juice, and avoid foods that contain high-fructose corn syrup or agave nectar.

A reasonable target is to limit fructose intake to about 20 grams per day.

This does not mean fruit is the enemy. It means the form, dose, and context matter. Whole fruit in moderate amounts is not the same thing as drinking fruit juice or consuming processed foods sweetened with concentrated fructose sources.

Sugar affects more than body weight. It can influence mitochondrial function, dopamine signaling, oxidative stress, gut health, inflammation, and energy metabolism. Since all of those systems matter for the brain, sugar is not something we should think about only through the lens of calories.

If the goal is better brain health, better energy, and better metabolic function, reducing excess sugar, especially concentrated fructose, is one of the simplest places to start.