It has long been known that polycystic ovarian syndrome (PCOS) is driven largely by chronically elevated insulin (hyperinsulinemia). PCOS is the most common endocrine abnormality among reproductive age women, affecting as much as 10% of the population (1). But if insulin is primarily a “blood sugar hormone,” why would chronic hyperinsulinemia affect female fertility? Why would it contribute to irregular or absent menstrual periods, facial hair, acne, and other signs and symptoms of PCOS?
The answer is that insulin is not just a blood sugar hormone. In fact, insulin has such surprising and far-reaching effects throughout the whole body that lowering blood sugar might actually be one of the least notable things this hormone does.
In a past KetoDiet post exploring chronic hyperinsulinemia, I mentioned that high insulin plays a driving role in such diverse issues as hypertension, skin tags, gout, and migraines. A quick flip through a biochemistry or endocrinology textbook shows that hormones don’t exist in a vacuum. They interact with and influence each other in complex ways, with multiple control mechanisms and feedback loops, so that changing the levels of one inevitably causes changes in the levels of others, too.
If hyperinsulinemia produces multiple hormonal abnormalities in women leading to PCOS, might it also produce hormonal abnormalities in men? Is there a male equivalent to PCOS?
Insulin Isn’t the Enemy; Chronically High Insulin Is
Insulin has gotten a very negative reputation in the keto community. But by itself, insulin isn’t a bad thing. Insulin is an essential hormone that performs numerous critical functions.
Insulin is only a problem when there’s too much of it in the bloodstream too often. Just like water, or even oxygen, it’s possible to get too much of a good thing. Insulin isn’t the enemy. For example, if you want to put on healthy muscle mass, you need insulin. But you don’t need a flood of it circulating in your body all the time. Keeping it pulsatile—that is, rising now and then for short periods of time—is sufficient for this purpose. What we want to avoid are prolonged periods of sustained high insulin.
Association Versus Causation
In medical research, the phrase “associated with” is often used when researchers are wary of using the term “causes.” It’s not always straightforward to establish cause and effect between two things with absolute certainty, so when things tend to occur together, it’s more scientifically responsible to say those things are “associated,” rather than declaring that one or more of them causes the others. However, in the case of PCOS, researchers believe that chronic hyperinsulinemia is a causative factor:
“Hyperinsulinemia associated with insulin resistance has been causally linked to all features of the syndrome, such as hyperandrogenism, reproductive disorders, acne, hirsutism and metabolic disturbances.” (2)
In fact, this causal link between hyperinsulinemia and PCOS is so well-known and so powerful that metformin — which is best known as a diabetes drug — is among the frontline pharmaceutical interventions for PCOS. As we’ll see soon, metformin and other diabetes drugs are also now being used for certain men’s health issues for the same reason — these issues stem from chronically elevated insulin.
The signs and symptoms of PCOS are driven by the underlying hormonal disturbances, which, apart from elevated insulin, include increased adrenal androgen synthesis (higher levels of testosterone and/or DHEA), decreased sex hormone binding globulin, increased luteinizing hormone (LH), and decreased follicle stimulating hormone (FSH). All of these features have also been observed in men, leading researchers to believe that yes, there is indeed a male hormonal equivalent of PCOS, and it has interesting repercussions for men of all ages (3).
And while many women with PCOS are overweight or obese, as many as 50% of PCOS patients are not (4). So it stands to reason that men with the male equivalent of PCOS won’t all be overweight, nor will they be diabetic, as defined by high blood sugar level. In PCOS and the male equivalent — just as in so many other chronic conditions — high blood glucose isn’t the driving factor; it’s high insulin.
Let’s look at three men’s health issues that seem to be coming from chronic hyperinsulinemia:
- Androgenetic alopecia (a.k.a. “male pattern baldness”)
- Erectile dysfunction
- Benign prostate hypertrophy (enlargement of the prostate gland)
Male-Pattern Baldness: Does Insulin Affect Hair Loss in Men?
Why do so many men lose their hair? Is it solely genetic? If someone comes from a long line of men who lost their hair, are they destined to lose theirs, too? If so, what would the evolutionary advantage to this be?
After all, many genetic conditions that have persisted throughout the ages are believed to have conferred a survival advantage in the distant past. For example, the sickle-shaped red blood cells produced by the genes responsible for sickle cell anemia also offer some degree of protection against malaria, so it makes sense that even though there’s a drawback to these genes in the modern age, in the past, it offered a distinct advantage. If there is an evolutionary advantage to men losing their hair, it hasn’t been identified yet. What has been identified, however, is a role for chronic hyperinsulinemia in contributing to male pattern baldness.
At first glance, you might think of male balding as an aesthetic issue and not a health problem. And no one could blame you for thinking it’s solely about appearance, rather than an underlying health issue. But looking at the role of insulin here tells us that for men losing their hair, things are more than “skin deep.”
The role of chronically elevated insulin as a contributor to male pattern baldness seems especially pronounced in young men. In fact, some researchers believe that in some men, hair loss might be the only warning sign of hyperinsulinemia.
An analysis of hormonal profiles in young men with early-onset androgenetic alopecia (AGA) (5) showed that compared to men without alopecia, young men with the condition had higher fasting insulin, HOMA-IR (a measurement of insulin resistance), and triglycerides, with slightly higher BMI, and lower HDL. All of these indicate that the men with AGA were affected more strongly by insulin. The study authors wrote, “Early-onset AGA might represent a phenotypic sign of the male PCOS-equivalent.”
In a case-control study of young men (age 19-30) presenting with AGA and 32 controls (men without AGA), mean fasting insulin levels were only slightly higher in the men with AGA than in those without it. However, compared with the controls, the men with AGA had significantly higher mean levels of testosterone, DHEA-sulfate and luteinizing hormone, with decreased mean levels of FSH and SHBG — precisely some of the same observations seen in women with PCOS.
The study conclusion couldn’t have said it better: “Men with early AGA could be considered as male phenotypic equivalents of women with PCOS. They can be at risk of developing the same complications associated with PCOS, including obesity, metabolic syndrome, IR [insulin resistance], cardiovascular diseases, and infertility.”(6)
It seems early male pattern baldness is more of a metabolic issue than a cosmetic one. The conclusion could have been written differently, though, with the arrow of causality pointing in the other direction: rather than saying men with AGA are at greater risk for metabolic syndrome and IR, it might be more educational to say that men with insulin resistance and metabolic syndrome are at greater risk for early baldness.
But how does this work? Is the connection between insulin resistance and early onset AGA merely an “association,” or is there a plausible mechanism by which causation can be established?
According to a paper written (7) by well-known Paleo diet authority Loren Cordain, PhD, along with low-carb advocates Drs. Michael and Mary Dan Eades, authors of Protein Power:
“Male balding clearly has a genetic component. However, it is well established that male pattern balding also is an androgen-dependent trait that occurs from elevated androgenesis after puberty. Consequently, any environmental factor or factors that would elevate serum androgen levels would promote increased balding, particularly in genetically susceptible individuals. High-glycemic-load carbohydrates, by inducing hyperinsulinemia, along with a concomitant elevation of serum androgens and reduction in SHBG represent a likely environmental agent that may in part underlie the promotion of male vertex balding.”
So it seems there is a genetic component to male balding. Obviously, not all men with hyperinsulinemia lose their hair, and not all men who are balding are hyperinsulinemic. Among young men with a genetic propensity for alopecia, chronic hyperinsulinemia simply increases the chances that they’ll lose their hair, compared to men of the same age who also have this genetic propensity but who are not hyperinsulinemic. The oft-uttered phrase regarding modern non-communicable health issues seems apropos here: “Genetics loads the gun, but diet and lifestyle pull the trigger.”
Other researchers have proposed a mechanism more specific to hair follicles, themselves, rather than a downstream effect of altered androgen hormone levels. The contend that insulin resistance “plays a pathogenetic role in the miniaturization of hair follicles.”(8) They go on to say that hyperinsulinemia causes alterations in blood vessel function that result in adverse effects on local circulation affecting the hair follicles, leading to a shrinking of follicles and eventual hair loss.
Another case/control study comparing groups of young men with early-onset AGA (9) and unaffected controls showed that compared to the men without hair loss, the men with AGA had higher fasting glucose, insulin, HOMA-IR, triglycerides, and blood pressure, all of which are suggestive of chronic hyperinsulinemia (10).
Unfortunately, the two groups were not matched for weight. Waist circumference, body weight, and BMI were all higher in the men with alopecia. This might have confounded the findings in that the higher weights could have been a contributing factor, but it could just as easily be true that higher insulin in the affected men was driving the higher body weight and waist circumference. That is, higher insulin may have been responsible for the higher weight, larger waist circumference, and the alopecia.
In case you needed another bit of evidence that there’s at the very least a correlation between male pattern baldness and insulin resistance, another study found that HOMA-IR was significantly higher in cases of men with early onset AGA than in men without alopecia (11).
For a nice change of pace, the authors of this one recognized the important implications: they recommend that young men with AGA be screened for insulin resistance and cardiovascular disease, writing, “Epidemiological studies have associated androgenetic alopecia (AGA) with severe young-age coronary artery disease and hypertension, and linked it to insulin resistance.” Of course, it would be wiser to simply make fasting insulin a standard part of routine bloodwork, right along with fasting glucose, which would then provide the HOMA-IR as well.
Men shouldn’t have to wait until they lose their hair before they’re told they’re at risk for the very serious complications of metabolic syndrome — including cardiovascular disease.
As just discussed, researchers believe young men with early onset male pattern baldness are at increased risk for coronary artery disease and hypertension, and suggest they should be screened for cardiovascular disease (CVD). With this in mind, it’s crucial to note that erectile dysfunction (ED) doesn’t result from lack of sexual desire. It’s not a libido problem, it’s a cardiovascular problem. And cardiovascular problems are largely insulin problems. CVD is not driven by high cholesterol or dietary saturated fat! (12)
Chronically high insulin — even when blood glucose is normal — is very damaging to the blood vessels. When combined with high blood glucose levels, it’s the perfect storm. Damage to the microscopic blood vessels in the eyes and the kidneys leads to the retinopathy and nephropathy that are well known consequences of poorly managed type 2 diabetes. But it’s not just those tiny blood vessels that suffer. The larger ones — major arteries — take a beating, too. In fact, cardiovascular disease is the number one cause of death in people with type 2 diabetes (13).
Impaired circulation also affects blood flow to the male genitalia. In fact, physicians informed on the hyperinsulinemic basis of blood vessel disfunction posit that ED may be the first sign of insulin resistance and endothelial dysfunction (14). This is especially true among younger men, who would not otherwise be suspected of having poor cardiovascular health. Make no mistake: erectile dysfunction and cardiovascular disease are different manifestations of the same underlying pathology (15). ED can be considered an early warning indicator of CVD.
Additionally, insulin resistance has been shown to reduce the synthesis and release of a compound called nitric oxide. Nitric oxide is a “vasodilator” — it helps blood vessels dilate so they can accommodate increased blood flow. In the vessels that supply blood to the penis, no dilation and no increased blood flow means no erection.
A systematic review looking at the association between erectile dysfunction and cardiovascular disease concluded, “ED and CVD should be regarded as two different manifestations of the same systemic disorder.” (15) And signs point to that systemic disorder being chronic hyperinsulinemia.
For a young man with no other signs and symptoms of metabolic derangement, erectile dysfunction could be the canary in the coalmine — an early warning sign that something is awry long before severe cardiovascular disease or type 2 diabetes have developed. One study found that in men under 40, compared to men without ED, those with ED had significantly higher HOMA-IR and systolic blood pressure. The researchers wrote, “Subclinical endothelial dysfunction and insulin resistance may be the underlying pathogenesis of ED in young patients without well-known etiology.” (16) In other words, for young men dealing with ED that has no known cause, insulin resistance should be suspected.
If the man/men in your life experience ED that has no obvious cause (such as depression, chronic stress, or physical trauma), or you are a man experiencing unexplained ED, a fasting insulin test might be warranted.
The incidence of various cardiovascular risk factors in 283 young ED patients (ages 18-45, with ED history at least 6 months). Insulin resistance (IR) is the most prevalent risk factor for ED in this study population. (17)
Metformin for Erectile Dysfunction: Why a Diabetes Drug?
It’s noteworthy that metformin — mainly a diabetes drug — has been shown to improve erectile function among insulin resistant men with ED who are not diagnosed diabetics (18). Why would a diabetes drug have any influence on erectile function if there was no connection to insulin or blood glucose? In a randomized, double-blind trial, compared to placebo, metformin led to significant improvements in HOMA-IR and erectile function. These two things are not unrelated! Based on the research we’ve explored here, it makes sense that better insulin management leads to better erectile function.
Benign Prostate Hypertrophy/Hyperplasia (BPH)
BPH is likely another condition with a surprising foundation in chronic hyperinsulinemia, but most men and even their physicians are unaware of this connection. Men are told, “You’re just getting older. This is normal.” It may be common, but that doesn’t mean it’s normal.
Insulin is a growth-promoting hormone. It stimulates growth of adipose tissue (fat cells), muscle tissue, and even the aforementioned skin tags and ovarian cysts. Another tissue insulin promotes growth of is the prostate gland (19). This finding, which is well documented in the scientific literature, has not yet made its way to the offices of many primary care physicians.
This is unfortunate, because these doctors are the ones most likely to encounter men complaining of the associated signs and symptoms, which include frequent or urgent need to urinate, waking up during the night to urinate, pain or straining during urination, or inability to completely empty the bladder.
One study showed that among men with BPH, fasting insulin levels were positively correlated with annual increase in growth rate of the prostate gland: the higher the insulin, the faster the growth (20). Prostate growth was faster in men with type-2 diabetes, hypertension, and obesity, all signs of hyperinsulinemia. In another study that compared 90 BPH patients and 90 men without the condition, levels of insulin and two other hormones, IGF-1 and estradiol, were higher in the cases compared to the controls. (Insulin may upregulate an enzyme called aromatase, which converts testosterone to estrogen/estradiol.) The researchers found that insulin and the related hormonal imbalances predicted the prostate size in patients with BPH: the higher the insulin, the larger the prostate (22).
Diabetes Drugs for BPH
As shown for erectile dysfunction, metformin has a therapeutic role in BPH. In rats with prostate enlargement induced by hyperinsulinemia (which is telling in itself—they gave rats insulin for the express purpose of enlarging their prostates!), treatment with the diabetes drug pioglitazone reduced insulin levels and prostate weight (23).
In a study looking at cultured human prostate cells in vitro, metformin substantially inhibited the proliferation of human prostate epithelial cells (24). Since these were a rat study and an in vitrostudy, we can’t be sure the same effects would be seen in human males, but the findings can still provide some insights.
Again, the fact that drugs primarily used for diabetes are effective for things as seemingly unrelated as PCOS, erectile dysfunction, and BPH, suggests these three conditions share a common origin: chronic hyperinsulinemia.
Take Home Message
It’s time to realize that type 2 diabetes and obesity are merely the tip of a much bigger iceberg of modern health issues rooted in chronically high insulin. Maybe it’s even time for a new acronym: MIRS—male insulin resistance syndrome.
If you’re a man dealing with problems known or suspected to be driven by chronic hyperinsulinemia, consider adopting a ketogenic diet or low-carb diet to bring your insulin levels down. Considering the amazing keto-friendly food you can eat when you reduce your carb intake, getting healthy never tasted so good!
Intermittent fasting is another strategy that can help improve insulin levels, and regular exercise may also be beneficial (25).
Source: Article by Amy Berger, MS, CNS, NTP (https://ketodietapp.com/Blog/lchf/hyperinsulinemia-and-mens-health-is-there-a-male-equivalent-to-pcos)
It’s the human diet. One size really does fit all.
When it comes to diet, it is often said that one size does not fit all. Different people fare better on different diets. I demur on this: one size — with a few personalized tweaks here and there — really does fit all. That may not be a popular stance, but I shall now set out the case for the defence.
Throughout the course of evolution many species of humans have roamed this globe, often coexisting. How strange it must have been, to occasionally encounter those “others.” But today we are alone, the last remaining species belonging to the Homo genus, which emerged over two million years ago. Sapiens is literally the last Homo standing.
Meet the family
When in 2003 the mapping of the human genome was completed, the heartening discovery was made that we are all related to each other. We modern humans can trace our origins to East Africa, our ancestral homeland. That is where Homo sapiens appeared, 200,000–300,000 years ago. We began to move into Asia something like 50,000–80,000 years ago. Before you knew it, we were everywhere, and doing a remarkable job of adapting and surviving.
The genes we carry today were determined in Africa. We are little changed since the end of the Paleolithic era, which represents 99.5% of human history. Our ancient genome has an average mutation rate of 0.5% per million years, meaning it “still resides for the greater part in the Paleolithic era.”
And so to food, and what to eat.
In order to answer that, we need to understand the “nutritional milieu” in which the genetic make-up of H. sapiens was established.
That is not to say that we should all be eating what is often referred to as the “Paleo” diet. Essentially, there is no such thing. Much of our success as a species can be ascribed to our adaptability to whatever environment we settled in as we migrated away from our original homeland. The menu varied wildly.
The out-of-Africa exodus occurred primarily along coastlines and rivers, and from lake to lake across North Africa. Consequently, anatomically modern humans regularly consumed fish and shellfish, high in protein and providing the micronutrients that are crucial for brain growth and development, including the fatty acid DHA, iodine and vitamins D and B12.
Meat was a dietary staple, especially for those who migrated further inland, providing high quality protein and fat, and highly bioavailable minerals, including iron and zinc. Skeletal analysis — the study of fossil isotopes — makes evident that “..even very early hominids consumed a considerable proportion of meat in their diets.”
The further north of the equator humans travelled, the less plant food was consumed, as it became less available.
Whatever their environment, all wild animals eat in accordance with the practice of “optimal foraging”. Optimal foraging is a behaviour whereby energy (calories) obtained from food must be greater than the amount of energy expended procuring that food.
Optimal foraging is about efficiency. You can’t spend all day, and all your energy, gathering a few leafy greens and berries when you have a hungry tribe back at camp to feed. Even today, hunter-gatherers show a strong preference for animal-based foods over plant-based foods, even when living in vegetation-rich environments.
That would also explain the attraction of junk food: lots of filling calories for little expenditure. It fits the paradigm of modern optimal foraging perfectly.
Our first mistake
In 1987, scientist and author Jared Diamond published his now famous article in Discover magazine, entitled The Worst Mistake in the History of the Human Race. He was talking about the first Agricultural Revolution that began around 10,000 years ago, when sapiens transitioned from a hunter-gathering to a settled, farming lifestyle. In his article he states:
“In particular, recent discoveries suggest that the adoption of agriculture, supposedly our most decisive step toward a better life, was in many ways a catastrophe from which we have never recovered.”
Agriculture changed the course of history, arguably more than any other human-driven event. The Neolithic era was characterised by a (gradual) switch from a highly varied, meat-based diet to a monotonous, cereal-based diet. A typical farmer’s diet in Neolithic Europe consisted mostly of bread made from wheat or other grains like rye and barley, supplemented with peas and lentils, milk and cheese, some occasional meat, and seasonal fruits.
The transition from a meat-based to a cereal-based diet resulted in numerous detrimental health effects, including reduction in stature, increase in infant mortality, reduction in lifespan, increase in iron deficiency anaemia, dental decay and bone mineral disorders, including osteomalacia.
Much-reduced protein consumption was a major feature of the Neolithic and contributed to a process called gracilization (thinning) of the skeleton. Pre-agricultural people had much greater bone density than we do today.
The Agricultural Revolution was one thing. Then came the Industrial Revolution, thousands of years later, but just seven or eight generations ago.
The Industrial Revolution gave rise to a completely new source of human nutrition: the processed food industry.
Since the start of the twentieth century, sugar consumption has rocketed, as has vegetable oil consumption, having largely replaced the animal fats traditionally used as a cooking medium. These novel vegetable oils are ubiquitous in processed foods. They are rich in omega-6 fatty acids that compete with, and displace, omega-3 fats (DHA) in the brain. Fish is the major source of DHA, and fish consumption has plummeted to levels well below the recommended amount in both the UK and the US.
As this extraordinary nutrition transition permeated the twentieth century, so too did its running mate, the disease transition.
Until the early 20th century, infectious diseases such as tuberculosis were the main cause of death following the post Neolithic era. By the mid 20th century, chronic diseases (diabetes, obesity, heart disease, cancer) had emerged as the number one threat to global health. Mental illnesses have increased in line with physical chronic diseases since 1960.
There has also been a transition in the advice we are expected to follow. Instead of consuming the diet that humans ate throughout evolution, experts now tell us to avoid or cut down on meat and saturated fats such as butter, and switch to those new, refined vegetable oils and cereal grains.
The 2017 U.S. Department of Agriculture report, US Trends in Food Availability, reveals that Americans have complied well with official dietary guidelines. Between 1970 and 2014, red meat consumption decreased by 28%, with overall saturated fat consumption down 27%. At the same time, vegetable cooking oil consumption rose by a staggering 248%. Consumption of grains, in the form of wheat flour, rice, corn, oats and barley, increased by 28%. Americans still consume 83% more than the recommended limit of 12.5 teaspoons of sugar per day.
Along with chronic diseases, something else is starting to surface, something less visible but arguably more sinister. The human brain is shrinking, as confirmed by a body of research that has been accumulating since 1988. This shrinkage — atrophy — began during the Epipaleolithic period, which was the transitional period between hunter-gathering and agriculture, and remains an ongoing phenomenon. Over the last 20,000 years, average brain size has decreased by 10%. What’s even more alarming is that the last 4,000–6,000 years have witnessed an acceleration of this atrophy.
Various theories have been proposed to explain this startling development, but no one cause has been established. I would hazard a guess that diet is involved.
If we assume that our current dietary habits are killing us, it surely makes scientific sense to take a close look at the overall health and diets of modern tribal peoples whose lifestyles remain largely uninfluenced by the western world.
Their way of life is under threat, which means we are all under threat. According to Survival International, the global organization that advocates on behalf of tribal peoples, “…tribal peoples are better at looking after their environment than anyone else.”
“Uncontacted peoples are supreme conservationists with the lightest footprint on our planet, and they protect some of the world’s last and most biodiverse forests. They have developed extraordinary skills and have unrivalled knowledge of their universe.” (Fiona Watson, Survival International)
We can learn from tribal peoples, but we need to be quick; most today are in transition between their traditional lifestyles and modern living.
Hair and blood analyses have shown that before the 1960s, the nutritional status of various tribal peoples (the !Kung, the Aka of the Central African Republic, aboriginal Australians and the northern European Sami) were within healthy ranges.
Approximately 15 years later, following settlement, these people had started to experience high rates of iron deficiency anaemia. Post-transition deficiencies in folate, iron, vitamins A, E and B12 were also observed, alongside an increase in diabetes, obesity, cardiovascular risk and cancer.
The nutrition transition phenomenon works in reverse. A paper published in 2009 in the European Journal of Clinical Nutrition detailed a small study that investigated the effect of a diet, similar to that consumed by preagricultural hunter-gatherers, on sedentary, slight overweight adult Americans. After following the diet for just ten days, all the volunteers experienced dramatic improvements in health markers, including “significant reductions” in blood pressure, improved arterial flexibility, improved insulin sensitivity, and lower blood fat levels. The diet consisted of lean meats, vegetables, fruits and nuts, and excluded cereals, dairy and legumes.
“Considerable evidence suggests that many common diseases can be prevented by hunter-gatherer diets.”(Lindeberg 2009)
In 1985, anthropologists S Boyd Eaton and Melvin J Konner proposed their “discordance hypothesis”, which states that the human genome is determined by the conditions of the Paleolithic era, and that changes have occurred too rapidly for us to adapt, resulting in a mismatch that leads to chronic disease.
“The physical activity, sleep, sun exposure, and dietary needs of every living organism (including humans) are genetically determined. This is why it is being increasingly recognized in the scientific literature, especially after Eaton and Konner’s seminal publication in 1985, that the profound changes in diet and lifestyle that occurred after the Neolithic Revolution (and more so after the Industrial Revolution and the Modern Age) are too recent on an evolutionary time scale for the human genome to have fully adapted.” (Carrera Bastos et al)
There is no one diet that characterises pre-agricultural humans, who ate from a fabulously broad menu, according to geographical location. However, there were commonalities. These include:
- High wild meat/fish intake with a preference for fatty prey
- Rare consumption of cereal grains
- No added sugar
- No refined vegetable oils
- Extensive range of wild plant foods, where available.
We cannot go back to a hunter-gatherer lifestyle — there are way too many of us, and in any case we lack the skills to do so. And who would choose to? But if some cataclysmic event (which may be coming) left us with no choice, we in the post-industrial world would not survive for long. We really do need to learn some ancient skills from tribal peoples.
The catch-22 dilemma is that neither can we continue to consume a diet that is making us sick, shrinking our brains and shortening our lives. We need to eat in a way that most closely resembles the diet on which we evolved. And is realistic.
There are several popular diets that fit this paradigm: the ketogenic diet, the Paleo diet, the Atkins diet, the ancestral diet, the low GI (glycaemic index) diet. Perhaps you could add a few more. Like the pre-agricultural diet of humans living all around the globe, these diets have their differences and their similarities. Paleo adherents don’t eat dairy foods, because they are a product of agriculture, and a recent addition to the human diet. Ketogenic fans love dairy foods, because they are so full of saturated fat.
But whatever their differences, all these diets are based on a low carbohydrate, high fat and/or protein way of eating, without sugary snacks and other processed “food”. And they are all as close as we can realistically get to the pre-agricultural diets of our ancestors, the one to which we are genetically adapted.
We Homo sapiens all require exactly the same nutrients, the same ones we’ve always needed. How much depends on age, level of physical activity, exposure to sunlight, geographical location, and so on. Some people have allergies or sensitivities to certain foods that they need to avoid. But nobody needs sugar, cereal grasses, vegetable oils et al.
As members of the Homo sapiens species, we all thrive on the same range of foods. You could call it the human diet.
Our technologically-driven, industry-centric lifestyles have left the vast majority of the global population so disconnected from the natural world that we can no longer see or understand our place within it. We live and think outside our natural context, and even accept absurd claims, such as fake meat substitutes, assembled in laboratories and factories, being healthier than the real thing. We choose foods that are nutrient-poor, and then buy factory-produced supplements to compensate for the shortfall.
You can change your diet as often as you like, and your food-based ideology. But you cannot change human evolutionary biology. One, broad-ranging size really does fit all.
Source: Article by Maria Cross MSc (https://medium.com/@mariacross/you-only-need-one-diet-ee5a676074e0)