Growth hormone may rise 300 percent with exercise: Acute increases also occur in cortisol, adrenaline, and noradrenaline

The figure below (click to enlarge) is from the outstanding book Physiology of sport and exercise, by Jack H. Wilmore, David L. Costill, and W. Larry Kenney. If you are serious about endurance or resistance exercise, or want to have a deeper understanding of exercise physiology beyond what one can get in popular exercise books, this book should be in your personal and/or institutional library. It is one of the most comprehensive textbooks on exercise physiology around. The full reference to the book is at the end of this post.

The hormonal and free fatty acid responses shown on the two graphs are to relatively intense exercise combining aerobic and anaerobic components. Something like competitive cross-country running in an area with hills would lead to that type of response. As you can see, cortisol spikes at the beginning, combining forces with adrenaline and noradrenaline (a.k.a. epinephrine and norepinephrine) to quickly increase circulating free fatty acid levels. Then free fatty acid levels are maintained elevated by adrenaline, noradrenaline, and growth hormone. As you can see from the graphs, free fatty acid levels are initially pulled up by cortisol, and then are very strongly correlated with adrenaline and noradrenaline.  Those free fatty acids feed muscle, and also lead to the production of ketones, which provide extra fuel for muscle tissue.

Growth hormone stays flat for about 40 minutes, after which it goes up steeply. At around the 90-minute mark, it reaches a level that is quite high; 300 percent higher than it was prior to the exercise session. Natural elevation of circulating growth hormone through intense exercise, intermittent fasting, and restful sleep, leads to a number of health benefits. It helps burn abdominal fat, often hours after the exercise session, and helps builds muscle (in conjunction with other hormones, such as testosterone). It appears to increase insulin sensitivity in the long run. Maybe natural elevation of circulating growth hormone is one of the “secrets” of people like Bob Delmonteque, who is probably the fittest octogenarian in the world today.

Aerobic activities normally do not elevate growth hormone levels, even though they are healthy, unless they lead to a significant degree of glycogen depletion. Glycogen is stored in the liver and muscle, with muscle storing about 5 times more than the liver (about 500 g in adults). Once those reserves go down significantly during exercise, it seems that growth hormone is recruited to ramp up fat catabolism and facilitate other metabolic processes. Walking for an hour, even if briskly, is good for fat burning, but generates only a small growth hormone elevation. Including a few all-out sprints into that walk can help significantly increase growth hormone secretion.

Having said that, it is not really clear whether growth hormone elevation is a response to glycogen depletion, or whether both happen together in response to another stimulus or related metabolic process. There are other factors that come into play as well. For example, circulating growth hormone increase is moderated by sex hormone (e.g., testosterone, estrogen) secretion, thus larger growth hormone increases in response to exercise are observed in older men than in older women. (Testosterone declines more slowly with age in men than estrogen does in women.) Also, growth hormone increase seems to be correlated with an increase in circulating ketones.

Heavy resistance exercise seems to lead to a higher growth hormone elevation per unit of time than endurance exercise. That is, an intense resistance training session lasting only 30 minutes can lead to an acute circulating growth hormone response, similar to that shown on the figure. The key seems to be reaching the point during the exercise where muscle glycogen stores are significantly depleted. Many people who weight-train achieve this regularly by combining a reasonable number of sets (e.g., 6-12), with repetitions in the muscle hypertrophy range (again, 6-12); and progressive overload, whereby resistance is increased incrementally every session.

Progressive overload is needed because glycogen reserves are themselves increased in response to training, so one has to increase resistance every session to keep up with those increases. This goes on only up to a point, a point of saturation, usually reached by elite athletes. Glycogen is the primary fuel for anaerobic exercise; fat is used as fuel in the recovery period between sets, and after the exercise is over. Glycogen is expended proportionally to the number of calories used in the anaerobic effort. Calories are expended proportionally to the total amount of weight moved around, and are also a function of the movements performed (moving a certain weight 1 feet spends less energy than moving it 3 feet). By the way, not much glycogen is depleted in a 30-minute session. The total caloric expenditure will probably be around 250 calories above the basal metabolic rate, which will require about 63 g of glycogen.

Many sensations are associated with reaching the glycogen depletion level required for an acute growth hormone response during heavy anaerobic exercise. Often light to severe nausea is experienced. Many people report a “funny” feeling, which is unmistakable to them, but very difficult to describe. In some people the “funny” feeling is followed, after even more exertion, by a progressively strong sensation of “pins and needles”, which, unlike that associated with a heart attack, comes slowly and also goes away slowly with rest. Some people feel lightheaded as well.

It seems that the optimal point is reached immediately before the above sensations become bothersome; perhaps at the onset of the “funny” feeling. My personal impression is that the level at which one experiences the “pins and needles” sensation should be avoided, because that is a point where your body is about to “force” you to stop exercising. (Note: I am not a bodybuilder; see “Interesting links” for more extensive resources on the subject.) Besides, go to that point or beyond and significant muscle catabolism may occur, because the body prioritizes glycogen reserves over muscle protein. It will break that protein down to produce glucose via gluconeogenesis to feed muscle glycogenesis.

That the body prioritizes muscle glycogen reserves over muscle protein is surprising to many, but makes evolutionary sense. In our evolutionary past, there were no selection pressures on humans to win bodybuilding tournaments. For our hominid ancestors, it was more important to have the glycogen tank at least half-full than to have some extra muscle protein. Without glycogen, the violent muscle contractions needed for a “fight or flight” response to an animal attack simply cannot happen. And large predators (e.g., a bear) would not feel intimated by big human muscles alone; it would be the human’s response using those muscles that would result in survival or death.

Overall, selection pressures probably favored functional strength combined with endurance, leading to body types similar to those of the hunter-gatherers shown on this post.

Even though the growth hormone response to exercise can be steep, the highest natural growth hormone spike seems to be the one that occurs at night, during deep sleep.

Exercising hard pays off, but only if one sleeps well.

Reference:

Wilmore, J.H., Costill, D.L., & Kenney, W.L. (2007). Physiology of sport and exercise. Champaign, IL: Human Kinetics.

Does Red Wine Protect the Cardiovascular System?

The 'French paradox' rears its ugly head again. The reasoning goes something like this: French people eat more saturated animal fat than any other affluent nation, and have the second-lowest rate of coronary heart disease (only after Japan, which has a much higher stroke rate than France). French people drink red wine. Therefore, red wine must be protecting them against the artery-clogging yogurt, beef and butter.

The latest study to fall into this myth was published in the AJCN recently (1). Investigators showed that 1/3 bottle of red wine per day for 21 days increased blood flow in forearm vessels of healthy volunteers, which they interpreted as "enhanced vascular endothelial function". The novel finding in this paper is that red wine consumption increases the migration of certain cells into blood vessels that are thought to maintain and repair the vessels. There were no control groups for comparison, neither abstainers nor a group drinking a different type of alcohol.

The investigators then went on to speculate that the various antioxidant polyphenols in red wine, such as the molecule resveratrol, could be involved. This could be true, but there's another possible mechanism here...

Ethanol-- plain old alcohol. You could drink a 40 oz bottle of malt liquor every night and it might do the same thing.

No matter what the source, alcohol consumption is associated with a lower risk of cardiovascular disease out to about 3-4 drinks per day, after which the risk goes back up (2, 3)*. The association is not trivial-- up to a 62% lower risk associated with alcohol use. Controlled trials have shown that alcohol, regardless of the source, increases HDL cholesterol and reduces the tendency to clot (4).

Should we all start downing three drinks a day? Not so fast. Although alcohol does probably decrease heart attack risk, the effect on total mortality is equivocal. That's because it increases the risk of cancers and accidents. Alcohol is a drug, and my opinion is that like all drugs, overall it will not benefit the health of a person with an otherwise good diet and lifestyle. That being said, it's enjoyable, so I have no problem with drinking it in moderation. Just don't think you're doing it for your health.

So does red wine decrease the risk of having a heart attack? Probably, yes, just like malt liquor does. I do think it's interesting to speculate about why alcohol (probably) reduces heart attack risk. Could it be because it relaxes us? I'm going to ponder that over a glass of whiskey...


* The first study is really interesting. For once, I see no evidence of "healthy user bias". Rates of healthy behaviors were virtually identical across quintiles of alcohol intake. This gives me a higher degree of confidence in the results.

Postprandial glucose levels, HbA1c, and arterial stiffness: Compared to glucose, lipids are not even on the radar screen

Postprandial glucose levels are the levels of blood glucose after meals. In Western urban environments, the main contributors to elevated postprandial glucose are foods rich in refined carbohydrates and sugars. While postprandial glucose levels may vary somewhat erratically, they are particularly elevated in the morning after breakfast. The main reason for this is that breakfast, in Western urban environments, is typically very high in refined carbohydrates and sugars.

HbA1c, or glycated hemoglobin, is a measure of average blood glucose over a period of a few months. Blood glucose glycates (i.e., sticks to) hemoglobin, a protein found in red blood cells. Red blood cells are relatively long-lived, lasting approximately 3 months. Thus HbA1c (given in percentages) is a good indicator of average blood glucose levels, if you don’t suffer from anemia or a few other blood abnormalities.

Based on HbA1c, one can then estimate his or her average blood glucose level for the previous 3 months or so before the test, using one of the following equations, depending on whether the measurement is in mg/dl or mmol/l.

Average blood glucose (mg/dl) = 28.7 × HbA1c − 46.7
Average blood glucose (mmol/l) = 1.59 × HbA1c − 2.59

Elevated blood glucose levels cause damage in the body primarily through glycation, which leads to the formation of advanced glycation endproducts (AGEs). Given this, HbA1c can be seen as a proxy for the level of damage done by elevated blood glucose levels to various body tissues. This damage occurs over time; often after many years of high blood glucose levels. It includes kidney damage, neurological damage, cardiovascular damage, and damage to the retina.

Most regular blood exams focus on fasting blood glucose as a measure of glucose metabolism status. Many medical practitioners have as a target a fasting blood glucose level of 125 mg/dl (7 mmol/l) or less, and largely disregard postprandial glucose levels or HbA1c in their management of glucose metabolism. Leiter and colleagues (2005; full reference at the end of this post) showed that this focus on fasting blood glucose is a mistake. They are not alone; many others made this point, including some very knowledgeable bloggers who focus on diabetes (see “Interesting links” section of this blog). Leiter and colleagues (2005) also provided some interesting graphs and figures, including eye-opening correlations between various variables and arterial stiffness. The figure below (click to enlarge) shows the contribution of postprandial glucose to HbA1c.

Note that the lower the HbA1c is in the figure (horizontal axis), the higher is the postprandial glucose contribution to HbA1c. And, the lower the HbA1c, the closer the individuals are to what one could consider having a perfectly normal HbA1c level (around 5 percent). That is, only for individuals whose HbA1c levels are very high, fasting blood glucose levels are relatively reliable measures of the tissue damage done be elevated blood glucose levels.

The table below (click to enlarge) shows P values associated with the impact of various variables (listed on the leftmost column) on arterial stiffness. This measure, arterial stiffness, is strongly associated with an increased risk of cardiovascular events. Look at the middle column showing P values adjusted for age and height. The lower the P value, the more a variable affects arterial stiffness. The variable with the lowest P value by far is 2-hour postprandial blood glucose; the blood glucose levels measured 2 hours after meals.

Fasting glucose levels were reported to be statistically insignificant because of the P = 0.049, in terms of their effect on arterial stiffness, but this P value is actually significant, although barely, at the 0.05 level (95 percent confidence). Interestingly, the following measures are not even on the radar screen, as far as arterial stiffness is concerned: systolic blood pressure, LDL cholesterol, HDL cholesterol, triglycerides, and fasting insulin levels.

What about the lipid hypothesis, and the “bad” LDL cholesterol!? This study is telling us that these are not very relevant for arterial stiffness when we control for the effect of blood glucose measures. Not even fasting insulin levels matters much! Wait, not even HDL!!! A high HDL has been definitely shown to be protective, but when we look at the relative magnitude of various effects, the story is a bit different. A high HDL’s protective effect exists, but it is dwarfed by the negative effect of high blood glucose levels, especially after meals, in the context of cardiovascular disease.

What all this points at is what we could call a postprandial glucose hypothesis: Lower your postprandial glucose levels, and live a longer, healthier life! And, by the way, if your postprandial glucose levels are under control, lipids do not matter much! Or maybe your lipids will fall into place, without any need for statin drugs, after your postprandial glucose levels are under control. One way or another, the outcome will be a positive one. That is what the data from this study is telling us.

How do you lower your postprandial glucose levels?

A good way to start is to remove foods rich in refined carbohydrates and sugars from your diet. Almost all of these are foods engineered by humans with the goal of being addictive; they usually come in boxes and brightly colored plastic wraps. They are not hard to miss. They are typically in the central aisles of supermarkets. The sooner you remove them from your diet, the better. The more completely you do this, the better.

Note that the evidence discussed in this post is in connection with blood glucose levels, not glucose metabolism per se. If you have impaired glucose metabolism (e.g., diabetes type 2), you can still avoid a lot of problems if you effectively control your blood glucose levels. You may have to be a bit more aggressive, adding low carbohydrate dieting (as in the Atkins or Optimal diets) to the removal of refined carbohydrates and sugars from your diet; the latter is in many ways similar to adopting a Paleolithic diet. You may have to take some drugs, such as Metformin (a.k.a. Glucophage). But you are certainly not doomed if you are diabetic.

Reference:

Leiter, L.A., Ceriello, A., Davidson, J.A., Hanefeld, M., Monnier, L., Owens, D.R., Tajima, N., & Tuomilehto, J. (2005). Postprandial glucose regulation: New data and new implications. Clinical Therapeutics, 27(2), S42-S56.

Sweet Potatoes

We can debate the nutritional qualities of a food until we're blue in the face, but in the end, we still may not have a very accurate prediction of the health effects of that food. The question we need to answer is this one: has this food sustained healthy traditional cultures?

I'm currently reading a great book edited by Drs. Hugh Trowell and Denis Burkitt, titled Western Diseases: Their Emergence and Prevention. It's a compilation of chapters describing the diet and health of traditional populations around the world as they modernize.

The book contains a chapter on Papua New Guinea highlanders. Here's a description of their diet:

A diet survey was undertaken involving 90 subjects, in which all food consumed by each individual was weighed over a period of seven consecutive days. Sweet potato supplied over 90 percent of their total food intake, while non-tuberous vegetables accounted for less than 5 percent of the food consumed and the intake of meat was negligible... Extensive herds of pigs are maintained and, during exchange ceremonies, large amounts of pork are consumed.

They ate no salt. Their calories were almost entirely supplied by sweet potatoes, with occasional feasts on pork.

How was their health? Like many non-industrial societies, they had a high infant/child mortality rate, such that 43 percent of children died before growing old enough to marry. Surprisingly, protein deficiency was rare. No obvious malnutrition was observed in this population, although iodine-deficiency cretinism occurs in some highlands populations:

Young adults were well built and physically fit and had normal levels of haemoglobin and serum albumin. Further, adult females showed no evidence of malnutrition in spite of the demands by repeated cycles of pregnancy and lactation. On the basis of American standards (Society of Actuaries, 1959), both sexes were close to 100 percent standard weight in their twenties.

The Harvard Pack Test carried out on 152 consecutive subjects demonstrated a high level of physical fitness which was maintained well into middle-age. Use of a bicycle ergometer gave an estimated maximum oxygen uptake of 45.2 ml per kilogram per minute and thus confirmed the high level of cardiopulmonary fitness in this group.

Body weight decreased with age, which is typical of many non-industrial cultures and reflects declining muscle mass but continued leanness.

There was no evidence of coronary heart disease or diabetes. Average blood pressure was on the high side, but did not increase with age. Investigators administered 100 gram glucose tolerance tests and only 3.8 percent of the population had glucose readings above 160 mg/dL, compared to 21 percent of Americans. A study of 7,512 Papuans from several regions with minimal European contact indicated a diabetes prevalence of 0.1 percent, a strikingly low rate. For comparison, in 2007, 10.7 percent of American adults had diabetes (1).

I'm not claiming it's optimal to eat nothing but sweet potatoes. But this is the strongest evidence we're going to come by that sweet potatoes can be eaten in quantity as part of a healthy diet. However, I wish I knew more about the varieties this group ate. Sweet potatoes aren't necessarily sweet. Caribbean 'boniato' sweet potatoes are dry, starchy and off-white. In the US, I prefer the yellow sweet potatoes to the orange variety of sweet potato labeled 'yams', because the former are starchier and less sweet. If I could get my hands on locally grown boniatos here, I'd eat those, but boniatos are decidedly tropical.

Instead, I eat potatoes, but I'm reluctant to recommend them whole-heartedly because I don't know enough about the traditional cultures that consumed them. I believe there are some low-CHD, low-obesity African populations that eat potatoes as part of a starch-based diet, but I haven't looked into it closely enough to make any broad statements. Potatoes have some nutritional advantages over sweet potatoes (higher protein content, better amino acid profile), but also some disadvantages (lower fiber, lower in most micronutrients, toxic glycoalkaloids).

Intermittent fasting, engineered foods, leptin, and ghrelin

Engineered foods are designed by smart people, and the goal is not usually to make you healthy; the goal is to sell as many units as possible. Some engineered foods are “fortified” with the goal of making them as healthy as possible. The problem is that food engineers are competing with many millions of years of evolution, and evolution usually leads to very complex metabolic processes. Evolved mechanisms tend to be redundant, leading to the interaction of many particles, enzymes, hormones etc.

Natural foods are not designed to make you eat them nonstop. Animals do not want to be eaten (even these odd-looking birds below). Most plants do not “want” their various nutritious parts to be eaten. Fruits are exceptions, but plants do not want one single individual to eat all their fruits. That compromises seed dispersion. Multiple individual fruit eaters enhance seed dispersion. Plants "want" one individual animal to eat some of their fruits and then move on, so that other individuals can also eat.

(Source: Teamsugar.com)

It is safe to assume that doughnut manufacturers want one single individual to eat as many doughnuts as possible, and many individuals to want to do that. That takes some serious food engineering, and a lot of testing. Success will increase the manufacturers' revenues, the real bottom line for them. The medical establishment will then take care of those individuals, and prolong their miserable lives so that they can continue eating doughnuts for as long as possible. It is self-perpetuating system.

As mentioned in this previous post, to succeed in the practice of intermittent fasting, one has to stop worrying about food, and one good step in that direction is to avoid engineered foods. In this sense, intermittent fasting can be seen as a form of liberation. Doing something enjoyable and forgetting about food. Like children playing outdoors; they do not care as much about food as they do about play. Even sleeping will do; most people forget about eating when they are asleep.

Intermittent fasting as a religious and/or social activity, as in the Great Lent and Ramadan, also seems to work well. Any activity that brings people together with a common goal, especially if the goal is not to do something evil, has a lot of potential for success.

If you approach intermittent fasting as another thing to worry about, then it will be tough – one fast per week, on the same day of the week, from 7.33 pm of one day to 3.17 pm of the next day. I exaggerate a bit. Anyway, if you approach it as another obligation, another modern stressor, you will probably fail in the medium to long term. It is just commonsense. Maybe you will be able to do it for a while, but not for long enough to reap some serious benefits. A few fasts are not going to make you lose a lot of weight; the body will adapt in a compensatory way during the fast, slowing down your metabolism a bit and conserving calories. On top of that, you will feel very, very hungry. That will make you binge when you break your fast. Compensatory adaptation (a very general phenomenon) is something that our body is very good at, regardless of what we want it to do.

From a more pragmatic perspective, for most people it is easier to fast at night and in the morning. Eating a big meal right after you wake up is not a very natural activity; several hormones that promote body fat catabolism are often elevated in the morning, causing mild physiological insulin resistance.

If you have dinner at 7 pm, skip breakfast, and then have brunch the next day at 10 am, you will have fasted for 15 h. If you skip breakfast and brunch, and have lunch at noon the next day, you will have fasted for 17 h.

On the other hand, if you have breakfast at 8 am, skip lunch, and then have dinner at 6 pm, you will have fasted only for 10 h.

Leptin levels seem to go down significantly after 12 h of fasting, leading to increased body fat catabolism and leptin sensitivity. This is a good thing, since leptin resistance seems to frequently precede insulin resistance.

Many people think that skipping breakfast will make them fat, for various reasons, including that being what sumo wrestlers do to put on enormous amounts of body fat. Well, skipping breakfast probably will make people fat if, when they break the fast, they stuff themselves to the point of almost throwing up, combine plenty of easily digestible carbohydrates (e.g., multiple bowls of rice) with a lot of dietary fat, and then go to sleep. That is what sumo wrestlers normally do.

Eating fat is great, but not together with lots of easily digestible carbohydrates. Even eating a lot of fat by itself will make it difficult for you to shed enough fat to look like the hunter-gatherers in this post. But your body fat set point will be much lower if you eat a lot of fat by itself than if you eat a lot of fat with a lot of easily digestible carbohydrates.

Anyway, if people skip breakfast and eat what they normally eat at lunch, they will not gain more body fat than they would have if they had breakfast. If they do anything to boost their metabolism in the morning, they will most certainly lose body fat in a noticeable way over several weeks, as long as they have enough fat to lose. For example, they can add some light activity in the morning (such as walking), or have a metabolism-boosting drink (e.g., coffee, green tea), or both.

Our hunter-gatherer ancestors, living outdoors, probably spent most of their day performing light activities that involved little stress. Those activities increase metabolism and fat burning, while keeping stress hormone levels at low ranges. Hunger suppression was the result, making intermittent fasting fairly easy.

Again, intermittent fasting should be approached as a form of liberation. You are no longer a slave of food.

It helps staying away from engineered foods as much as possible, because, again, they are usually engineered with food addiction in mind. I am talking primarily about foods rich in refined carbohydrates and sugars. They come in boxes and plastic bags with labels describing calories and macronutrient composition, which are often wrong or misleading.

Let us say we could transport a group of archaic Homo sapiens to a modern city, and feed them white bread, bagels, doughnuts, potato chips industrially fried in vegetable oils, and the like. Would they say “Yuck, how can these people eat this?” No, they would not. It would be heaven for them; they would want nothing else for the rest of their gustatorily happy but health-wise miserable lives.

While practicing intermittent fasting, it is probably a good idea to have fixed meal times, and skipping them from time to time. The reason is the hunger hormone ghrelin, secreted by the stomach (mostly) and pancreas to stimulate hunger and possibly prepare the digestive tract for optimal or quasi-optimal absorption of food. Its secretion appears to follow the pattern of habitual meals adopted by a person.

References:

Elliott, W.H., & Elliott, D.C. (2009). Biochemistry and molecular biology. 4th Edition. New York: NY: Oxford University Press.

Fuhrman, J., & Barnard, N.D. (1995). Fasting and eating for health: A medical doctor's program for conquering disease. New York, NY: St. Martin’s Press.

Pastured Dairy may Prevent Heart Attacks

Not all dairy is created equal. Dairy from grain-fed and pasture-fed cows differs in a number of ways. Pastured dairy contains more fat-soluble nutrients such as vitamin K2, vitamin A, vitamin E, carotenes and omega-3 fatty acids. It also contains more conjugated linoleic acid, a fat-soluble molecule that has been under intense study due to its ability to inhibit obesity and cancer in animals. The findings in human supplementation trials have been mixed, some confirming the animal studies and others not. In feeding experiments in cows, Dr. T. R. Dhiman and colleagues found the following (1):

Cows grazing pasture and receiving no supplemental feed had 500% more conjugated linoleic acid in milk fat than cows fed typical dairy diets.

Fat from ruminants such as cows, sheep and goats is the main source of CLA in the human diet. CLA is fat-soluble. Therefore, skim milk doesn't contain any. It's also present in human body fat in proportion to dietary intake. This can come from dairy or flesh.

In a recent article from the AJCN, Dr. Liesbeth Smit and colleagues examined the level of CLA in the body fat of Costa Rican adults who had suffered a heart attack, and compared it to another group who had not (a case-control study, for the aficionados). People with the highest level of CLA in their body fat were 49% less likely to have had a heart attack, compared to those with the lowest level (2).

Since dairy was the main source of CLA in this population, the association between CLA and heart attack risk is inextricable from the other components in pastured dairy fat. In other words, CLA is simply a marker of pastured dairy fat intake in this population, and the (possible) benefit could just as easily have come from vitamin K2 or something else in the fat.

This study isn't the first one to suggest that pastured dairy fat may be uniquely protective. The Rotterdam and EPIC studies found that a higher vitamin K2 intake is associated with a lower risk of heart attack, cancer and overall mortality (3, 4, 5). In the 1940s, Dr. Weston Price estimated that pastured dairy contains up to 50 times more vitamin K2 than grain-fed dairy. He summarized his findings in the classic book Nutrition and Physical Degeneration. This finding has not been repeated in recent times, but I have a little hunch that may change soon...

Vitamin K2
Cardiovascular Disease and Vitamin K2
Can Vitamin K2 Reverse Arterial Calcification?

Atheism is a recent Neolithic invention: Ancestral humans were spiritual people

For the sake of simplicity, this post treats “atheism” as synonymous with “non-spiritualism”. Technically, one can be spiritual and not believe in any deity or supernatural being, although this is not very common. This post argues that atheism is a recent Neolithic invention; an invention that is poorly aligned with our Paleolithic ancestry.

Our Paleolithic ancestors were likely very spiritual people; at least those belonging to the Homo sapiens species. Earlier ancestors, such as the Australopithecines, may have lacked enough intelligence to be spiritual. Interestingly, often atheism is associated with high intelligence and a deep understanding of science. Many well-known, and brilliant, evolution researchers are atheists (e.g., Richard Dawkins).

Well, when we look at our ancestors, spirituality seems to have emerged as a result of increased intelligence.

Spirituality can be seen in cave paintings, such as the one below, from the Chauvet Cave in southern France. The Chauvet Cave is believed to have the earliest known cave paintings, dating back to about 30 to 40 thousand years ago. The painting below is on the cover of the book Dawn of art: The Chauvet Cave. (See the full reference for this publication and others at the end of this post.)

The most widely accepted theory of the origin of cave paintings is that they were used in shamanic or religious rituals. By and large, they were not used to convey information (e.g., as maps); and they are often found deep in caves, in areas that are almost inaccessible, ruling out a “decorative” artistic purpose. As De La Croix and colleagues (1991) note:

Researchers have evidence that the hunters in the caves, perhaps in a frenzy stimulated by magical rites and dances, treated the painted animals as if they were alive. Not only was the quarry often painted as pierced by arrows, but hunters actually may have thrown spears at the images, as sharp gouges in the side of the bison at Niaux suggest.

Niaux is another cave in southern France. Like the Chauvet Cave, it is full of prehistoric paintings. Even though those paintings are believed to be more recent, dating back to the end of the Paleolithic, they follow the same patterns seen almost everywhere in prehistoric art. The patterns point at a life that gravitates around spiritual rituals.

Isolated hunter-gatherers also provide a glimpse at our spiritual Paleolithic past. No isolated hunter-gatherer group has ever been found in which atheism was the predominant belief among its members. In fact, the life of most isolated hunter-gatherer groups that have been studied appears to have revolved around religious rituals. In many of these groups, shamans held a very high social status, and strongly influenced group decisions.

Finally, there is solid empirical evidence from human genetics and the study of modern human groups that: (a) “religiosity” may be coded into our genes, to a larger extent in some individuals than in others; and (b) those who are spiritual, particularly those who belong to a spiritual or religious group, have generally better health and experience lower levels of depression and stress (which likely influence health) than those who do not.

There was once an ape that became smart. It invented weapons, which greatly multiplied the potential for death and destruction of the ape’s natural propensity toward violence; violence often motivated by different religious and cultural beliefs held by different groups. It also invented delicious foods rich in refined carbohydrates and sugars, which slowly poisoned the ape’s body.

Could the recent invention of atheism have been just as unhealthy?

Surely religion has been at the source of conflicts that have caused much death and destruction. But is religion, or spirituality, really to be blamed? Many other factors can lead to a great deal of death and destruction, sometimes directly, other times indirectly – e.g., poverty and illiteracy.

References:

Brown, D.E. (1991). Human universals. New York, NY: McGraw-Hill.

Chauvet, J.M., Deschamps, E.B., & Hillaire, C. (1996). Dawn of art: The Chauvet Cave. New York, NY: Harry N. Abrams.

De La Croix, H., Tansey, R.G., & Kirkpatrick, D. (1991). Gardner’s art through the ages: Ancient, medieval, and non-European art. Philadelphia, PA: Harcourt Brace.

Gombrich, E.H. (2006). The story of art. London, England: Pheidon Press.

Murdock, G.P. (1958). Outline of world cultures. New Haven, CN: Human Relations Area Files Press.