Monday, November 20, 2017

We share an ancestor who probably lived no more than 640 years ago


We all evolved from one single-celled organism that lived billions of years ago. I don’t see why this is so hard for some people to believe, given that all of us also developed from a single fertilized cell in just 9 months.

However, our most recent common ancestor is not that first single-celled organism, nor is it the first Homo sapiens, or even the first Cro-Magnon.

The majority of the people who read this blog probably share a common ancestor who lived no more than 640 years ago. Genealogical records often reveal interesting connections - the figure below has been cropped from a larger one from Pinterest.


You and I, whoever you are, have each two parents. Each of our parents have (or had) two parents, who themselves had two parents. And so on.

If we keep going back in time, and assume that you and I do not share a common ancestor, there will be a point where the theoretical world population would have to be impossibly large.

Assuming a new generation coming up every 20 years, and going backwards in time, we get a theoretical population chart like the one below. The theoretical population grows in an exponential, or geometric, fashion.


As we move back in time the bars go up in size. Beyond a certain point their sizes go up so fast that you have to segment the chart. Otherwise the bars on the left side of the chart disappear in comparison to the ones on the right side (as several did on the chart above). Below is the section of the chart going back to the year 1371.


The year 1371 is a little more than 640 years ago. (This post is revised from another dated a few years ago, hence the number 640.) And what is the theoretical population in that year if we assume that you and I have no common ancestors? The answer is: more than 8.5 billion people. We know that is not true.

Admittedly this is a somewhat simplistic view of this phenomenon, used here primarily to make a point. For example, it is possible that a population of humans became isolated 15 thousand years ago, remained isolated to the present day, and that one of their descendants just happened to be around reading this blog today.

Perhaps the most widely cited article discussing this idea is this one by Joseph T. Chang, published in the journal Advances in Applied Probability. For a more accessible introduction to the idea, see this article by Joe Kissell.

Estimates vary based on the portion of the population considered. There are also assumptions that have to be made based on migration and mating patterns, as well as the time for each generation to emerge and the stability of that number over time.

Still, most people alive today share a common ancestor who lived a lot more recently than they think. In most cases that common ancestor probably lived less than 640 years ago.

And who was that common ancestor? That person was probably a man who, due to a high perceived social status, had many consorts, who gave birth to many children. Someone like Genghis Khan.

Tuesday, October 24, 2017

Could the low testosterone problem be a mirage?


Low testosterone (a.k.a. “low T”) is caused by worn out glands no longer able to secrete enough T, right? At least this seems to be the most prevalent theory today, a theory that reminds me a lot of the “tired pancreas” theory () of diabetes. I should note that this low T problem, as it is currently presented, is one that affects almost exclusively men, particularly middle-aged men, not women. This is so even though T plays an important role in women’s health.

There are many studies that show associations between T levels and all kinds of diseases in men. But here is a problem with hormones: often several hormones vary together and in a highly correlated fashion. If you rely on statistics to reach conclusions, you must use techniques that allow you to rule out confounders; otherwise you may easily reach wrong conclusions. Examples are multivariate techniques that are sensitive to Simpson’s paradox and nonlinear algorithms; both of which are employed, by the way, by modern software tools such as WarpPLS (). Unfortunately, these are rarely, if ever, used in health-related studies.

Many low T cases may actually be caused by something other than tired T-secretion glands, perhaps a hormone (or set of hormones) that suppress T production; a T “antagonist”. What would be a good candidate? The figure below shows two graphs. It is from a study by Starks and colleagues, published in the Journal of the International Society of Sports Nutrition in 2008 (). The study itself is not directly related to the main point that this post tries to make, but the figure is.



Look at the two graphs carefully. The one on the left is of blood cortisol levels. The one on the right is of blood testosterone levels. Ignore the variation within each graph. Just compare the two graphs and you will see one interesting thing – cortisol and testosterone levels are inversely related. This is a general pattern in connection with stress-induced cortisol elevations, repeating itself over and over again, whether the source of stress is mental (e.g., negative thoughts) or physical (e.g., intense exercise).

And the relationship between cortisol and testosterone is strong. Roughly speaking, an increase in cortisol levels, from about 20 to 40 μg/dl, appears to bring testosterone levels down from about 8 to 5 ηg/ml. A level of 8 ηg/ml (the same as 800 ηg/dl) is what is normally found in young men living in urban environments. A level of 5 ηg/ml is what is normally found in older men living in urban environments.

So, testosterone levels are practically brought down to almost half of what they were before by that variation in cortisol.

Chronic stress can easily bring your cortisol levels up to 40 μg/dl and keep them there. More serious pathological conditions, such as Cushing’s disease, can lead to sustained cortisol levels that are twice as high. There are many other things that can lead to chronically elevated cortisol levels. For instance, sustained calorie restriction raises cortisol levels, with a corresponding reduction in testosterone levels. As the authors of a study () of markers of semistarvation in healthy lean men note, grimly:

“…testosterone (T) approached castrate levels …”

The study highlights a few important phenomena that occur under stress conditions: (a) cortisol levels go up, and testosterone levels go down, in a highly correlated fashion (as mentioned earlier); and (b) it is very difficult to suppress cortisol levels without addressing the source of the stress. Even with testosterone administration, cortisol levels tend to be elevated.

Isn't possible that cortisol levels go up because testosterone levels go down - reverse causality? Possible, but unlikely. Evidence that testosterone administration may reduce cortisol levels, when it is found, tends to be rather weak or inconclusive. A good example is a study by Rubinow and colleagues (). Not only were their findings based on bivariate (or unadjusted) correlations, but also on a chance probability threshold that is twice the level usually employed in statistical analyses; the level usually employed is 5 percent.

Let us now briefly shift our attention to dieting. Dieting is the main source of calorie restriction in modern urban societies; an unnatural one, I should say, because it involves going hungry in the presence of food. Different people have different responses to dieting. Some responses are more extreme, others more mild. One main factor is how much body fat you want to lose (weight loss, as a main target, is a mistake); another is how low you expect body fat to get. Many men dream about six-pack abs, which usually require single-digit body fat percentages.

The type of transformation involving going from obese to lean is not “cost-free”, as your body doesn’t know that you are dieting. The body “sees” starvation, and responds accordingly.

Your body is a little bit like a computer. It does exactly what you “tell” it to do, but often not what you want it to do. In other words, it responds in relatively predictable ways to various diet and lifestyle changes, but not in the way that most of us want. This is what I call compensatory adaptation at work (). Our body often doesn’t respond in the way we expect either, because we don’t actually know how it adapts; this is especially true for long-term adaptations.

What initially feels like a burst of energy soon turns into something a bit more unpleasant. At first the unpleasantness takes the form of psychological phenomena, which were probably the “cheapest” for our bodies to employ in our evolutionary past. Feeling irritated is not as “expensive” a response as feeling physically weak, seriously distracted, nauseated etc. if you live in an environment where you don’t have the option of going to the grocery store to find fuel, and where there are many beings around that can easily kill you.

Soon the responses take the form of more nasty body sensations. Nearly all of those who go from obese to lean will experience some form of nasty response over time. The responses may be amplified by nutrient deficiencies. Obesity would have probably only been rarely, if ever, experienced by our Paleolithic ancestors. They would have never gotten obese in the first place. Going from obese to lean is as much a Neolithic novelty as becoming obese in the first place, although much less common.

And it seems that those who have a tendency toward mental disorders (e.g., generalized anxiety, manic-depression), even if at a subclinical level under non-dieting conditions, are the ones that suffer the most when calorie restriction is sustained over long periods of time. Most reports of serious starvation experiments (e.g., Roy Walford’s Biosphere 2 experiment) suggest the surfacing of mental disorders and even some cases of psychosis.

Emily Deans has a nice post () on starvation and mental health.

But you may ask: What if my low T problem is caused by aging; you just said that older males tend to have lower T? To which I would reply: Isn’t possible that the lower T levels normally associated with aging are in many cases a byproduct of higher stress hormone levels? Take a look at the figure below, from a study of age-related cortisol secretion by Zhao and colleagues ().



As you can see in the figure, cortisol levels tend to go up with age. And, interestingly, the range of variation seems very close to that in the earlier figure in this post, although I may be making a mistake in the conversion from nmol/l to ηg/ml. As cortisol levels go up, T levels should go down in response. There are outliers. Note the male outlier at the middle-bottom part, in his early seventies. He is represented by a filled circle, which refers to a disease-free male.

Dr. Arthur De Vany claims to have high T levels in his 70s. It is possible that he is like that outlier. If you check out De Vany’s writings, you’ll see his emphasis on leading a peaceful, stress-free, life (). If money, status, material things, health issues etc. are very important for you when you are young (most of us, a trend that seems to be increasing), chances are they are going to be a major source of stress as you age.

Think about individual property accumulation, as it is practiced in modern urban environments, and how unnatural and potentially stressful it is. Many people subconsciously view their property (e.g., a nice car, a bunch of shares in a publicly-traded company) as their extended phenotype. If that property is damaged or loses value, the subconscious mental state evoked is somewhat like that in response to a piece of their body being removed. This is potentially very stressful; a stress source that doesn’t go away easily. What we have here is very different from the types of stress that our Paleolithic ancestors faced.

So, what will happen if you take testosterone supplementation to solve your low T problem? If your problem is due to high levels of cortisol and other stress hormones (including some yet to be discovered), induced by stress, and your low T treatment is long-term, your body will adapt in a compensatory way. It will “sense” that T is now high, together with high levels of stress.

Whatever form long-term compensatory adaptation may take in this scenario, somehow the combination of high T and high stress doesn’t conjure up a very nice image. What comes to mind is a borderline insane person, possibly with good body composition, and with a lot of self-confidence – someone like the protagonist of the film American Psycho.

Again, will the high T levels, obtained through supplementation, suppress cortisol? It doesn’t seem to work that way, at least not in the long term. In fact, stress hormones seem to affect other hormones a lot more than other hormones affect them. The reason is probably that stress responses were very important in our evolutionary past, which would make any mechanism that could override them nonadaptive.

Today, stress hormones, while necessary for a number of metabolic processes (e.g., in intense exercise), often work against us. For example, serious conflict in our modern world is often solved via extensive writing (through legal avenues). Violence is regulated and/or institutionalized – e.g., military, law enforcement, some combat sports. Without these, society would break down, and many of us would join the afterlife sooner and more violently than we would like (see Pinker’s take on this topic: ).

Sir, the solution to your low T problem may actually be found elsewhere, namely in stress reduction. But careful, you run the risk of becoming a nice guy.

Friday, September 29, 2017

Gaining muscle and losing fat at the same time: Various issues and two key requirements

In a previous post (), I mentioned that the idea of gaining muscle and losing fat at the same time seems impossible to most people because of three widely held misconceptions: (a) to gain muscle you need a calorie surplus; (b) to lose fat you need a calorie deficit; and (c) you cannot achieve a calorie surplus and deficit at the same time.

The scenario used to illustrate what I see as a non-traumatic move from obese or seriously overweight to lean is one in which weight loss and fat loss go hand in hand until a relatively lean level is reached, beyond which weight is maintained constant (as illustrated in the schematic graph below). If you are departing from an obese or seriously overweight level, it may be advisable to lose weight until you reach a body fat level of around 21-24 percent for women or 14-17 percent for men. Once you reach that level, it may be best to stop losing weight, and instead slowly gain muscle and lose fat, in equal amounts. I will discuss the rationale for this in more detail in my next post; this post will focus on addressing the misconceptions above.


Before I address the misconceptions, let me first clarify that, when I say “gaining muscle” I do not mean only increasing the amount of protein stored in muscle tissue. Muscle tissue is mostly water, by far. An important component of muscle tissue is muscle glycogen, which increases dramatically with strength training, and also tends to increase the amount of water stored in muscle. So, when you gain muscle, you gain a significant amount of water.

Now let us take a look at the misconceptions. The first misconception, that to gain muscle you need a calorie surplus, was dispelled in a previous post featuring a study by Ballor and colleagues (). In that study, obese subjects combined strength training with a mild calorie deficit, and gained muscle. They also lost fat, but ended up a bit heavier than at the beginning of the intervention. Another study along the same lines was linked by Clint (thanks) in the comments section under the last post ().

The second misconception, that to lose fat you need a calorie deficit; is related to the third, that you cannot achieve a calorie surplus and deficit at the same time. In part these misconceptions are about semantics, as most people understand “calorie deficit” to mean “constant calorie deficit”. One can easily vary calorie intake every other day, generating various calorie deficits and surpluses over a week, but with no overall calorie deficit or surplus for the entire week. This is why I say that one can achieve a calorie surplus and deficit “at the same time”. But let us make a point very clear, most of the evidence that I have seen so far suggests that you do not need a calorie deficit to lose fat, but you do need a calorie deficit to lose structural weight (i.e., non-water weight). With a few exceptions, not many people will want to lose structural weight by shedding anything other than body fat. One exception would be professional athletes who are already very lean and yet are very big for the weight class in which they compete, being unable to "make weight" through dehydration.

Perhaps the most surprising to some people is that, based on my own experience and that of several HCE () users, you don’t even need to vary your calorie intake that much to gain muscle and lose fat at the same time. You can achieve that by eating enough to maintain your body weight. In fact, you can even slowly increase your calorie intake over time, as muscle growth progresses beyond the body fat lost. And here I mean increasing your calorie intake very slowly, proportionally to the amount of muscle you gain; which also means that the incremental increase in calorie intake will vary from person to person. If you are already relatively lean, at around 21-24 percent of body fat for women and 14-17 percent for men, gaining muscle and losing fat in equal amounts will lead to a visible change in body composition over time () ().

Two key requirements seem to be common denominators for most people. You must eat protein regularly; not because muscle tissue is mostly protein, but because protein seems to act as a hormone, signaling to muscle tissue that it should repair itself. (Many hormones are proteins, actually peptides, and also bind to receptor proteins.) And you also must conduct strength training to the point that you are regularly hitting the supercompensation window (). This takes a lot of individual customization (). You can achieve that with body weight exercises, although free weights and machines seem to be generally more effective. Keep in mind that individual customization will allow you to reach your "sweet spots", but that still results will vary across individuals, in some cases dramatically.

If you regularly hit the supercompensation window, you will be progressively spending slightly more energy in each exercise session, chiefly in the form of muscle glycogen, as you progress with your strength training program. You will also be creating a hormonal mix that will increase the body’s reliance on fat as a source of energy during recovery. As a compensatory adaptation (), your body will gradually increase the size of its glycogen stores, raising insulin sensitivity and making it progressively more difficult for glucose to become body fat.

Since you will be progressively spending slightly more energy over time due to regularly hitting the supercompensation window, that is another reason why you will need to increase your calorie intake. Again, very slowly, proportionally to your muscle gain. If you do not do that, you will provide a strong stimulus for autophagy () to occur, which I think is healthy and would even recommend from time to time. In fact, one of the most powerful stimuli to autophagy is doing strength training and fasting afterwards. If you do that only occasionally (e.g., once every few months), you will probably not experience muscle loss or gain, but you may experience health improvements as a result of autophagy.

The human body is very adaptable, so there are many variations of the general strategy above.

Thursday, September 7, 2017

PLS Applications Symposium; 11 - 13 April 2018; Laredo, Texas


PLS Applications Symposium; 11 - 13 April 2018; Laredo, Texas
(Abstract submissions accepted until 15 February 2018)

*** Health researchers ***

The research techniques discussed in this Symposium are finding growing use among health researchers. This is in part due to steady growth in the use of the software WarpPLS (visit: http://warppls.com) among those researchers. For those interested in learning more, a full-day workshop will be conducted (see below).

*** Only abstracts are needed for the submissions ***

The partial least squares (PLS) method has increasingly been used in a variety of fields of research and practice, particularly in the context of PLS-based structural equation modeling (SEM). The focus of this Symposium is on the application of PLS-based methods, from a multidisciplinary perspective. For types of submissions, deadlines, and other details, please visit the Symposium’s web site:

http://plsas.net

*** Workshop on PLS-SEM ***

On 11 April 2018 a full-day workshop on PLS-SEM will be conducted by Dr. Ned Kock and Dr. Geoffrey Hubona, using the software WarpPLS. Dr. Kock is the original developer of this software, which is one of the leading PLS-SEM tools today; used by thousands of researchers from a wide variety of disciplines, and from many different countries. Dr. Hubona has extensive experience conducting research and teaching topics related to PLS-SEM, using WarpPLS and a variety of other tools. This workshop will be hands-on and interactive, and will have two parts: (a) basic PLS-SEM issues, conducted in the morning (9 am - 12 noon) by Dr. Hubona; and (b) intermediate and advanced PLS-SEM issues, conducted in the afternoon (2 pm - 5 pm) by Dr. Kock. Participants may attend either one, or both of the two parts.

The following topics, among others, will be covered - Running a Full PLS-SEM Analysis - Conducting a Moderating Effects Analysis - Viewing Moderating Effects via 3D and 2D Graphs - Creating and Using Second Order Latent Variables - Viewing Indirect and Total Effects - Viewing Skewness and Kurtosis of Manifest and Latent Variables - Viewing Nonlinear Relationships - Solving Collinearity Problems - Conducting a Factor-Based PLS-SEM Analysis - Using Consistent PLS Factor-Based Algorithms - Exploring Statistical Power and Minimum Sample Sizes - Exploring Conditional Probabilistic Queries - Exploring Full Latent Growth - Conducting Multi-Group Analyses - Assessing Measurement Invariance - Creating Analytic Composites.

-----------------------------------------------------------
Ned Kock
Symposium Chair
http://plsas.net

Sunday, August 27, 2017

Sudden cholesterol increase? It may be psychological


There are many published studies with evidence that cholesterol levels are positively associated with heart disease. In multivariate analyses the effects are usually small, but they are still there. On the other hand, there is also plenty of evidence that cholesterol is beneficial in terms of health. Here of course I am referring to the health of humans, not of the many parasites that benefit from disease.

For example, there is evidence () that cholesterol levels are negatively associated with mortality (i.e., higher cholesterol leading to lower mortality), and are positively associated with vitamin D production from skin exposure to sunlight ().

Most of the debris accumulated in atheromas are made up of macrophages, which are specialized cells that “eat” cell debris (ironically) and some pathogens. The drug market is still hot for cholesterol-lowering drugs, often presented in TV and Internet ads as effective tools to prevent formation of atheromas.

But what about macrophages? What about calcium, another big component of atheromas? If drugs were to target macrophages for atheroma prevention, drug users may experience major muscle wasting and problems with adaptive immunity, as macrophages play a key role in muscle repair and antibody formation. If drugs were to target calcium, users may experience osteoporosis.

So cholesterol is the target, because there is a “link” between cholesterol and atheroma formation. There is also a link between the number of house fires in a city and the amount of firefighting activity in the city, but we don’t see mayors announcing initiatives to reduce the number of firefighters in their cities to prevent house fires.

When we talk about variations in cholesterol, we usually mean variations in cholesterol carried by LDL particles. That is because LDL cholesterol seems to be very “sensitive” to a number of factors, including diet and disease, presenting quite a lot of sudden variation in response to changes in those factors.

LDL particles seem to be intimately involved with disease, but do not be so quick to conclude that they cause disease. Something so widespread and with so many functions in the human body could not be primarily an agent of disease that needs to be countered with statins. That makes no sense.

Looking at the totally of evidence linking cholesterol with health, it seems that cholesterol is extremely important for the human body, particularly when it is under attack. So the increases in LDL cholesterol associated with various diseases, notably heart disease, may not be because cholesterol is causing disease, but rather because cholesterol is being used to cope with disease.

LDL particles, and their content (including cholesterol), may be used by the body to cope with conditions that themselves cause heart disease, and end up being blamed in the process. The lipid hypothesis may be a classic case of reverse causation. A case in point is that of cholesterol responses to stress, particularly mental stress.

Grundy and Griffin () studied the effects of academic final examinations on serum cholesterol levels in 2 groups of medical students in the winter and spring semesters (see table below). During control periods, average cholesterol levels in the two groups were approximately 213 and 216 mg/dl. During the final examination periods, average cholesterol levels were 248 and 240 mg/dl. These measures were for winter and spring, respectively.



One could say that even the bigger increase from 213 to 248 is not that impressive in percentage terms, approximately 16 percent. However, HDL cholesterol does not go up significantly in response to sustained (e.g., multi-day) stress, it actually goes down, so the increases reported can be safely assumed to be chiefly due to LDL cholesterol. For most people, LDL particles are the main carriers of cholesterol in the human body. Thus, in percentage terms, the increases in LDL cholesterol are about twice those reported for total cholesterol.

A 32-percent increase (16 x 2) in LDL cholesterol would not go unnoticed today. If one’s LDL cholesterol were to be normally 140 mg/dl, it would jump to 185 mg/dl with a 32-percent increase. It looks like the standard deviations were more than 30 in the study. (This is based on the standard errors reported, and assuming that the standard deviation equals the standard error multiplied by the square root of the sample size.) So we can guess that several people might go from 140 to 215 or more (this is LDL cholesterol, in mg/dl) in response to the stress from exams.

And the effects above were observed with young medical students, in response to the stress from exams. What about a middle-aged man or woman trying to cope with chronic mental stress for months or years, due to losing his or her job, while still having to provide for a family? Or someone who has just been promoted, and finds himself or herself overwhelmed with the new responsibilities?

Keep in mind that sustained dieting can be a major stressor for some people, particular when one gets to that point in the dieting process where he or she gets regularly into negative nitrogen balance (muscle loss). So you may have heard from people saying that, after months or years of successful dieting, their cholesterol levels are inexplicably going up. Well, this post provides one of many possible explanations for that.

The finding that cholesterol goes up with stress has been replicated many times. It has been known for a long time, with studies dating back to the 1950s. Wertlake and colleagues () observed an increase in average cholesterol levels from 214 to 238 (in mg/dl); also among medical students, in response to the mental and emotional stress of an examination week. A similar study to the one above.

Those enamored with the idea of standing up the whole day, thinking that this will make them healthy, should know that performing cognitively demanding tasks while standing up is a known stressor. It is often used in research where stress must be induced to create an experimental condition. Muldoon and colleagues () found that people performing a mental task while standing experienced an increase in serum cholesterol of approximately 22 points (in mg/dl).

What we are not adapted for is sitting down for long hours in very comfortable furniture (, ). But our anatomy clearly suggests adaptations for sitting down, particularly when engaging in activities that resemble tool-making, a hallmark of the human species. Among modern hunter-gatherers, tool-making is part of daily life, and typically it is much easier to accomplish sitting down than standing up.

Modern urbanites could be seen as engaging in activities that resemble tool-making when they produce things at work for internal or external customers, whether those things are tangible or intangible.

So, stress is associated with cholesterol levels, and particularly with LDL cholesterol levels. Diehard lipid hypothesis proponents may argue that this is how stress is associated with heart disease: stress increases cholesterol which increases heart disease. Others may argue that one of the reasons why LDL cholesterol levels are sometimes found to be associated with heart disease-related conditions, such as chronic stress, and other health conditions is that the body is using LDL cholesterol to cope with those conditions.

Specifically regarding mental stress, a third argument has been put forth by Patterson and colleagues, who claimed that stress-mediated variations in blood lipid concentrations are a secondary result of decreased plasma volume. The cause, in their interpretation, was unspecified – “vascular fluid shifts”. However, when you look at the numbers reported in their study, you still see a marked increase in LDL cholesterol, even controlling for plasma volume. And this is all in response to “10 minutes of mental arithmetic with harassment” ().

I tend to think that the view that cholesterol increases with stress because cholesterol is used by the body to cope with stress is the closest to the truth. Among other things, stress increases the body’s overall protein demand, and cholesterol is used in the synthesis of many proteins. This includes proteins used for signaling, also known as hormones.

Cholesterol also seems to be a diet marker, tending to go up in high fat diets. This is easier to explain. High fat diets increase the demand for bile production, as bile is used in the digestion of fat. Most of the cholesterol produced by the human body is used to make bile.

Monday, July 10, 2017

Hands-On Workshop on PLS-SEM with WarpPLS; 12-13 August 2017; Penang, Malaysia


Structural equation modeling (SEM), or path analysis with latent variables, is one of the most general and comprehensive statistical analysis methods. Path analysis, multiple regression, ANCOVA, ANOVA and other widely used statistical analysis methods can be seen as special cases of SEM.

SEM use employing WarpPLS has been growing steadily among researchers investigating health-related topics.

We will be conducting a two-day hands-on workshop on SEM employing partial least squares methods (PLS-SEM) with WarpPLS. This software conducts composite-based (e.g., PLS-based) as well as factor-based SEM analyses. Factor-based SEM combines the precision of covariance-based SEM with the flexibility and ease-of-use of composite-based SEM. The dates are 12-13 August 2017. The workshop will take place in Penang, Malaysia.

For more details, please go to:

http://bit.ly/2tZRLKX

or

https://warppls.blogspot.com/2017/07/hands-on-workshop-on-pls-sem-with.html

Friday, June 30, 2017

Eating fish whole: Sardines

Different parts of a fish have different types of nutrients that are important for our health; this includes bones and organs. Therefore it makes sense to consume the fish whole, not just filets made from it. This is easier to do with small than big fish.

Small fish have the added advantage that they have very low concentrations of metals, compared to large fish. The reason for this is that small fish are usually low in the food chain, typically feeding mostly on plankton, especially algae. Large carnivorous fish tend to accumulate metals in their body, and their consumption over time may lead to the accumulation of toxic levels of metals in our bodies.

One of my favorite types of small fish is the sardine. The photo below is of a dish of sardines and vegetables that I prepared recently. Another small fish favorite is the smelt (see this post). I buy wild-caught sardines regularly at the supermarket.


Sardines are very affordable, and typically available throughout the year. In fact, sardines usually sell for the lowest price among all fish in my supermarket; lower even than tilapia and catfish. I generally avoid tilapia and catfish because they are often farmed (tilapia, almost always), and have a poor omega-6 to omega-3 ratio. Sardines are rich in omega-3, which they obtain from algae. They have approximately 14 times more omega-3 than omega-6 fatty acids. This is an excellent ratio, enough to make up for the poorer ratio of some other foods consumed on a day.

This link gives a nutritional breakdown of canned sardines; possibly wild, since they are listed as Pacific sardines. (Fish listed as Atlantic are often farm-raised.) The wild sardines that I buy and eat probably have a higher vitamin and mineral content that the ones the link refers to, including higher calcium content, because they are not canned or processed in any way. Two sardines should amount to a little more than 100 g; of which about 1.6 g will be the omega-3 content. This is a pretty good amount of omega-3, second only to a few other fish, like wild-caught salmon.

Below is a simple recipe. I used it to prepare the sardines shown on the photo above.

- Steam cook the sardines for 1 hour.
- Spread the steam cooked sardines on a sheet pan covered with aluminum foil; use light olive oil to prevent the sardines from sticking to the foil.
- Preheat the oven to 350 degrees Fahrenheit.
- Season the steam cooked sardines to taste; I suggest using a small amount of salt, and some chili powder, garlic powder, cayenne pepper, and herbs.
- Bake the sardines for 30 minutes, turn the oven off, and leave them there for 1 hour.

The veggies on the plate are a mix of the following: sweet potato, carrot, celery, zucchini, asparagus, cabbage, and onion. I usually add spinach but I had none around today. They were cooked in a covered frying pan, with olive oil and a little bit of water, in low heat. The cabbage and onion pieces were added to the mix last, so that in the end they had the same consistency as the other veggies.

I do not clean, or gut, my sardines. Normally I just wash them in water, as they come from the supermarket, and immediately start cooking them. Also, I eat them whole, including the head and tail. Since they feed primarily on plant matter, and have a very small digestive tract, there is not much to be “cleaned” off of them anyway. In this sense, they are like smelts and other small fish.

For many years now I have been eating them like that; and so have my family and some friends. Other than some initial ew’s, nobody has ever had even a hint of a digestive problem as a result of eating the sardines like I do. This is very likely the way most of our hominid ancestors ate small fish.

If you prepare the sardines as above, they will be ready to store, or eat somewhat cold. There are several variations of this recipe. For example, you can bake the sardines for 40 minutes, and then serve them hot.

You can also add the stored sardines later to a soup, lightly steam them in a frying pan (with a small amount of water), or sauté them for a meal. For the latter I would recommend using coconut oil and low heat. Butter can also be used, which will give the sardines a slightly different taste.