Formulate Your Own Supplements

Generally, I don’t take supplements.  But when I do, I buy them in their pure, powdered form and encapsulate them myself. 

A supplement company does the same thing, only on a larger scale.  It acquires pure, powdered supplements from one of the few supplement manufacturers and packages them into dosage units (e.g. capsules or tablets).  Then, it bottles those dosage units into containers that bear the name of its company, before selling them, at a premium, to wholesalers and retailers.

Not only is doing it on your own cheaper, but it also allows you, the user, to decide on the type of dilutant[*] to use, as well as to avoid certain excipients that may be necessary on a large production scale, but unnecessary (and possibly allergenic) for making supplements at home for your own use.  You also get to create your own unique mixtures of supplements, and to vary the proportions of the supplements in those mixtures – handy for self-experimentation purposes.[†] And, lest the requirement for comprehensiveness be disregarded, some powdered supplements taste awful, so encapsulating them automatically gets around this taste factor.

Preserving Brain Function: Principles, Pitfalls, and Practical Conclusions

INTRODUCTION

I recently had the opportunity to attend a physician-only-lecture at a hospital about the use of ketogenic diets for the treatment of epilepsy in children.  If you at least casually follow the discourse on this dietary approach on the interwebz, especially with regard to the interest of effecting cures, you’d probably think that not only should all children with epilepsy be placed on a ketogenic diet, but that failing to do so amounts to nothing less than egregious malpractice; another failure of the medical profession to employ the best treatments available because of the inherent evils of pharmaceutical companies and of patent medicine.

The truth is, although there are a myriad of proposed mechanisms as far as how ketogenic diets work (review articles have been rapidly accumulating in many different medical publications) no one can really say one way or the other, and to suggest otherwise points to an utter lack of thoroughness in reading of the literature on the topic, a bias in the interpretation of said literature, or both.

Diet Dogma Rears Ugly Head Again: Become a Fat Burner, Eat Your Own Crap, and Live Longer

Holding my dog up against my chest moments before he had peacefully taken his last few breaths, I thought about how cold his hands and feet were; how slow his heart beat and breathing were; and just how much he had shrunk and atrophied.  Of course, these are all the consequences of aging, a topic that I try to avoid thinking about because thinking about aging leads to thinking about your own mortality, or the mortality of those close to you. 

A great amount of money is spent on things that could possibly delay the aging and the advent of the diseases associated with it, including hormone replacement therapy.  But this demented idea to meaningfully delay aging has spawned some dreadful ideas that have little basis in science. 

My Guest Post for 180 Degree Health

Rethinking our Diets -- 80/10/10 and Fruitarianism

Although I have a rule for myself to not read consumer books about diet or health, despite not having much free time of late, I couldn’t resist the opportunity to speed-read through 80/10/10 by Dr. Douglas Graham recently.

I wasn’t able to see what all the fuss was about, knowing perfectly well how popular 80/10/10 is becoming.  There was but not one thing specifically insightful or interesting to report here.  Instead, despite what’s said by Dr. Graham to the contrary, I found the book to be a rehashing of what natural hygienists (like Dr. Emmet Densmore) had put forth in the past – only presented in a way to support the idea that humans had evolved to thrive on a vegan diet, mainly of fruit and, on average, no more than 10 percent of calories from fat and protein and no less than 80 percent of calories from carbohydrate.

But that’s not the purpose of this post; that is, to point out the errors, oversights, and half-truths in 80/10/10 – of which there are many.  It is instead to urge a recalibration of how we should think about diets and the arguments that are put forth for them, so as to avoid the financial, emotional, and bodily harm already incurred by those who were in desperate need of help, and so willing to try anything.

Brain Food

"Fish is brain food," is what I would hear in college from a roommate of mine who was seriously into his health.  He believed this so much that he would eat a piece of fatty fish before exams, and would urge me to do the same.  I was interested in health at the time, too, so I tried it.  Maybe I just didn't do it right or for long enough because I found that my friend's pre-exam ritual was a bad one, as was his reasoning for doing so, which was a physiological impossibility.

There is an ever-present belief that if a food contains a substance that is found in a particular body part, it follows inevitably that said food is beneficial for said body part.  I think this is what people really mean when they say that fish is brain food.  The meat of fish and the brain both contain phosphorus, and before the hype about omega-3 fatty acids, phosphorus was thought to be the reason why fish was good for the brain.  Fish is actually a modest source of phosphorus, as there are many other foods that contain significantly more, and phosphorus is now known to be a minor element of brain tissue.

An Examination of Popular "Diets" -- Avoid Them All

Some of the dietary practices that are currently promoted have the inconvenience of producing some of the effects that these practices are being undertaken to check in the first place—namely cortisol and estrogen. 

If any person were so persuaded to do so, he or she should bear in mind that a deficiency of calories, carbohydrate, salt, calcium, and excessive amounts of histamine, choline, and prostaglandins are some of the factors that activate both cortisol and estrogen. 

I’ve written about stress and the reasons for keeping it as low as possible.  Refer back to those for context for this post.  But briefly, the stress hormones—cortisol, adrenalin, noradrenalin, growth hormone, glucagon, and some others—are all catabolic and estrogenic.  When they persist in the blood too long or excessively, irreversible degenerative processes are set in motion that affect all aspects and all levels of the body.

Protein, the Thyroid Gland, Metabolism, and Conceptions About Weight Loss Diets

I apologize for the long break but I hope to be back for a while.  I’ve been getting many emails and messages since my hiatus, and, I promise, I will try my best to get to all of them.  I really appreciate the kind words I’ve been receiving, and, if I may say so without presumption, see it as a good augury of success that I’m providing decent content.  Okay, onward. 

Regarding some of these messages, a theme all too familiar is gaining weight on restrictive diets, or not being able to eat “anything” without getting fatter.  I’m working on a guest post for Matt Stone’s site about this topic, and ways in which to overcome it, especially those who have been lifelong dieters or under-eaters.  One person emailed me recently saying that she could not eat more than about 700 calories per day without gaining weight.  This has been a matter of absorbing interest of mine of late, and I have some ideas I wish to delve into, but herein, I will briefly discuss the one macronutrient that, I think, almost everyone agrees is the least fattening of all the macronutrients: protein.

PUFA, Lipid Peroxidation Processes, and the Implications for Atherosclerosis and Diet Part III

Part I, II

Out of curiosity, using cronometer, I decided to see how much PUFA I was eating on a daily basis for a week.  It was tedious but, on average, I had consumed about 5 grams of PUFA a day, and substantially greater amounts of monounsaturated and saturated fats.  An essential fatty acid (EFA) deficiency is out of the question at this level, at least per the clinicial signs and symptoms, but I naturally began to wonder what my tissues would look like if I had been consuming much less PUFA, essentially depleting myself of linoleic acid (LA) and arachidonic acid (AA). 

It turns out that the synthesis and presence of eicosatrienoic acid (ETA), or mead acid, would increase, in proportion to the exclusion of the EFAs from the diet, and the appearance of ETA can occur in a matter of days.  You’ll seldom find information on ETA in textbooks and in searches on databases that index scientific articles, like PubMed, other than the fact that it serves as a marker for an EFA deficiency.  The mere presence of ETA is also usually taken as evidence that an EFA deficiency has caused, or contributed, to the condition that tends to coexist with it. 

But an EFA deficiency per se is not always at play, as there could be an inability to synthesize and desaturate fatty acids properly, in which case the addition of PUFA would probably provide benefit. (PUFA have indispensable signaling and structural functions, namely in the phospholipids that are found in cell membranes.)  Or, it could merely indicate an overall poor diet.

Lipid peroxidation, acne, and the complexity of nutrient interactions

Introduction:

I’m probably treading on thin ice here, but I’ve been thinking about why milk would cause acne in some people.  I have not the means of forming a solid judgment but initially, I was thinking offhand that the high calcium content in milk could be a factor.  Excess calcium impairs the absorption of zinc and a zinc deficiency depletes vitamin E and thus vitamin A.  Zinc and vitamin A are particularly protective against the development of acne.¹

I think this highlights how complex nutrient interactions can get as well as the importance of examining all possibilities and assumptions when we attempt to draw associations between two things.  It’s tempting to assume that one thing causes another simply because they regularly occur simultaneously, or one regularly occurs before the other in time.  Leaping to a cause and effect conclusion is easier and faster, no doubt, than to take due cares to investigate the relationship so as to rule out all possible alternative explanations. 

Many, unfortunately, do not shoulder such care—unintentionally or not.   But I leave this train of thought. 

Bacteria are often said to be the cause of acne but I’ve always had my doubts about this model.  Antibiotics—applied topically or taken orally—do in fact improve and prevent acne, sometimes quite dramatically, but I think the explanation as to how this happens lies outside the idea that antibiotics merely kill bacteria, P. acnes, present on the skin.  Lo and behold, bacteria are not unconditionally required for acne.²

The interplay among the human intestinal microbial landscape, obesity, metabolism, and nutritional status: an overview

INTRODUCTION 

I’ve been paying much more attention to the human intestinal microbial landscape because of the red meat-carnitine study, and more recently, this one.  There is a growing body of compelling evidence linking the types of bacteria that colonize our intestines, and therefore the types of toxins we are exposed to, and our risk of diseases that include obesity. 

I’ve written about this before, namely with respect to the gram-negative bacterial toxin, lipopolysaccharide (LPS), as it relates to physical attractiveness, as well as the apparent beneficial metabolic effects of sterilizing the intestines of all microbial life.

I don’t want to dwell on this matter, but I do want to try to delve further into the intricacies of the topic and the evidence in which many of the suppositions are based, and towards the end, shed light on some pathways that open up possibilities for intervention.

What I learned from the red meat-carnitine study (plus what I ate today)

The red meat-carnitine study¹ has made the rounds on the interwebz and many a blogger has had an opportunity to thoroughly deconstruct it, and, as usual, the data presented in the study did not, in any way, warrant the sensationalism and conclusion—that the consumption of red meat could lead to heart disease on the basis of its carnitine content—drawn by the press and media. (Though, the distinction that having “healthy” gut flora as opposed to normal or unhealthy would inhibit the conversion of carnitine to TMAO is lost on me.)

It was an easy one to swat down, but what was interesting to me was the fervor and vitriolic, yet laser sharp, scrutiny (and of course, all wrapped up with the obligatory pleas for critical thinking), with which this particular study was jumped on by the Paleo diet community in the defense of their sacred cow: red meat.

The inverse relationship between the quality assessment of a study and confirmation bias is ever present in science, and not necessarily wrong, but members of diet movements tend to take it to a level that ends up making me feel uncomfortable and nauseous.  It's simply human nature to scrutinize studies that tend to disagree with our preconceived beliefs more intensely than those that tend to agree with them, but this bias rears its ugly head so often and so blatantly in the Paleosphere so as to be reprehensible. 

PUFA, lipid peroxidation processes, and the implications for atherosclerosis and diet Part II

Please bear with me for this one, as I want to address a comment that was left on my blog regarding fish, namely how it exerts its beneficial effects.  Apparently, the folks over at PHD believe fish oil is beneficial by way of hormesis, which is the idea that the exposure to small doses of a toxin fortifies our resistance to it upon subsequent exposures.

In the case of fish oil, the previously mentioned decomposition products, derived mainly from DHA and EPA hydroperoxides, are the toxins that elicit hormetic responses.  Toxic in themselves, these lipid hydroperoxides are the starting material for a host of highly toxic decomposition products, including 4-hydroxyhexenal (4-HHE), which is the one that is usually evoked to discuss the potentially beneficial hormetic effect of fish oil.

4-HHE corresponds to 4-hydroxynonenal (4-HNE), which is generated from linoleic acid (LA) and arachidonic acid (AA).  Compared to 4-HNE, there have been fewer studies conducted with respect to the toxicity of 4-HHE.   However, I think it would be reasonable to assume, given their structural similarities, that 4-HNE and 4-HEE would produce similar effects in the body.  (2-hydroxyheptanal, also derived from LA, has similar effects to 4-HNE.)  Regardless, 4-HNE can be, and is probably, produced from EPA and DHA as well.¹

4-HNE is highly reactive and highly toxic, plain and simple.  It’s also physiologically relevant because LA and AA are the major PUFA found in mammalian tissue, especially in phospholipids and lipoproteins.  Aldehydes like these, and their oxidation products, like oxime and pyrazoline, have been found to accumulate in old age,² atherosclerosis, and inflammatory conditions like rheumatoid arthritis.³

PUFA, lipid peroxidation processes, and the implications for atherosclerosis and diet

I recently read on the interwebz that fish oil lowers triglyceride levels in the blood by depositing them in the arteries.  I have known about this triglyceride lowering effect, and whether I should be taking fish oil as a supplement as is recommended by major health organizations, alternative health practitioners, and my mom. 

As a whole, I think the clinical trial evidence for fish oil for the prevention and treatment of cardiovascular disease, especially of late, have been disappointing, to say the least, and this goes for the other conditions for which fish oil has been, for years now, said to benefit.  Fish oil does in reality lower triglycerides but what is the trade-off? 

Studies like this one by Angerer et al., for instance, in which subjects who were randomized to receive fish oil—1.65 grams of omega-3 fatty acids per day— or a placebo demonstrated, after two years, a greater degree of atherosclerosis in the carotid arteries of the subjects who had received fish oil compared to those who had received a placebo.¹

The presence of highly reactive methylene groups renders PUFA highly susceptible to peroxidation processes, and the more double bonds a PUFA molecule has, the greater the chance becomes.  As an example, DHA and EPA are more susceptible than arachidonic acid (AA), which are both more susceptible than linoleic acid (LA) and alpha linolenic acid (ALA) to lipid peroxidation processes.

Why cells go bad: a new appreciation and understanding of ATP opens up an untapped avenue for fighting diabetes, cancer, aging, etc.

It’s refreshing to see people beginning to think clearly and rationally and move away from gimmicky diets that have little basis in fact, reality, or objectivity, and to ones that are firmly seated in all aspects of human physiology and science.

After all, this is why most of us choose to eat a certain way, that is to be as healthy as we can be, both physically and mentally . . . not to, say, replicate how our caveman ancestors supposedly ate and lived.

It’s due to this line of reasoning that carbohydrates, and especially sugar and fructose, have fallen by the wayside of late, driven by an irrational fear, bordering on obsessiveness, that’s evolved to where sugar is now conceived of as a toxic poison and blamed for causing diabetes, cancer, obesity, gout, etc. (Thank you Dr. Lustig.)

It’s important to point out that sugar is used by virtually every cell in the body to generate energy, or ATP.  The brain is especially reliant on glucose for optimal functioning: The brain represents only 2 percent of the body’s total weight yet accounts for 15 percent of the body’s total energy expenditure. ¹ Indeed, the brain is a voracious sugar guzzler, and sugar, not ketone bodies, is its preferred fuel source, despite popular discourse to the contrary.  Insulin and sugar make us smarter ² so it stands to reason that ketosis has the opposite effect.

Diabetes, Dangerous Fat, and Protective Sugar

Since the discovery of the so-called “glucose-fatty acid cycle” in 1963, there has been more and more evidence accumulating linking free fatty acids with diabetes (Randle, Garland, Hales, & Newsholme, 1963).  Briefly, the glucose-fatty acid cycle describes a competition, whereby the use of glucose becomes impaired by the presence of fatty acids and, to a lesser extent, vice versa (Cook, King, & Veech, 1978). 

Others had hinted at this fatty acid-induced blocking effect of sorts before.  Among them, was a guy named Apollinaire Bouchardat, a French pharmacist, who gave his diabetic patients sweet fruit and bread made from gluten, and had good results.  Others had applied Bouchardat’s dietary prescription and achieved equally good success.  More recently, an English physician, William Budd, following on the heels of these pioneers, gave his diabetic patients around 8 ounces of sugar daily, with only the intent of slowing the cachexia that was characteristic of long-standing poorly controlled diabetes.  Not only did most of his patients stop wasting away, but they also began to stop losing sugar in their urine when given this “saccharine treatment” (Hughes, 1862).

Another prominent clinician-researcher, Harold Himsworth, who was also first to show that insulin sensitivity in the tissues is reduced in diabetics, decades later, suggested, based on his clinical experiences and a review of the population data that high intakes of dietary fat (which raises free fatty acid levels) caused diabetes, and that diets rich in carbohydrates and low in fat were protective of it (Himsworth, 1934a, 1934b, 1936).

Insulin revisited, cell physiology, membrane pumps, and internet commenters

In my first “fact check” of Dr. Ray Peat, I had discussed the mechanisms by which insulin exerts its effects from the conventional textbook point-of-view.  I’ve gotten mostly good feedback on that post, and some idiotic ones, from the people who obviously didn’t take the time to read it, or if they did failed to understand it.  

Briefly, the conventional view is that insulin, upon being secreted by the β-cells of the pancreatic islets, acts on and activates the insulin receptors, initiating the insulin-signaling cascade.  This activation of the insulin receptor then provides a docking site for the insulin receptor substrate (IRS) proteins, which thereafter activate kinases in the vicinity that contain a specific SH2 domain, namely the kinase that phosphorylates the 3-position of the membrane lipid phosphatidylinositol 4,5-bisphosphate (PI 3,4 P₂) to phosphatidylinositol 3,4,5-trisphosphate (PI 3,4,5 P₃).

Figure 1 Insulin signaling pathways in the cell. GLUT = glucose transporter (lower right)

This lipid product, PI 3,4,5 P₃ thereafter activates the kinase, PDK1, and PDK1 phosphorylates and activates Akt, another kinase that moves throughout the cell’s cytoplasm, executing most of insulin’s actions, the most important of which for this post is the translocation of the glucose transporters from the cytoplasm to the plasma membrane.

Thyroid Hormone, Desaturase Enzymes, and the Implications on Membranes and Energy Generation

Purely based on physical and chemical considerations, it’s becoming clear that higher   membrane saturation indices go hand in hand with longevity and a greater resistance to toxic substances like lipopolysaccharide.

The types of saturated fats and unsaturated fats, as well as the proportion of each in the cellular membranes, are governed largely by the types of fats ingested and the body’s nutritional status and hormonal milieu.  It’s been touched on previously on this blog but insulin, for instance, activates several desaturase enzymes, which explains why fats synthesized from carbohydrates, via DNL, consist of a mixture of saturated & monounsaturated fats.

(On the other hand, food restriction tends to increase the saturation indices of membranes, and not simply because food-restricted individuals are incidentally ingesting less unsaturated fats, as I’ve recently heard suggested off hand.)

These inherent processes, whereby saturated fats are converted to unsaturated fats, seem to be important for controlling the fluidity of cellular membranes so that enzymes, such as lipases, which only operate within a range of membrane viscosities, can act on cellular lipids.  Oxygen and the reducing equivalents, NADH & NADPH, are essential cofactors of the desaturase enzymes. (Fructose depletes NADH.)

Thyroid supplement users should take note of the fact that thyroid hormone tends to decrease the saturation indices of membranes.

The Half-Life of Human Fat Tissue is 600 Days?

In the 1940s, some of the toxic effects of fish oil (such as testicular degeneration, softening of the brain, muscle damage, and spontaneous cancer) were found to result from an induced vitamin E deficiency. Unfortunately, there isn't much reason to think that just supplementing vitamin E will provide general protection against the unsaturated fats. The half-life of fats in human adipose tissue is about 600 days, meaning that significant amounts of previously consumed oils will still be present up to four years after they have been removed from the diet.¹   - Dr. Ray Peat

If there was ever an adage passed around by Dr. Peat’s followers that’s left my head spinning, it’s this one.  Several people have so far asked me to comment on it so here we go.

Bear in mind that triglycerides are continuously being broken down into their component fatty acids and glycerol by the enzyme hormone-sensitive lipase (HSL), which is inhibited by insulin and activated by noradrenalin.  Some degree of lipolysis and reesterification is happening all the time.  This is called the triglyceride-fatty acid cycle.²

Dr. Peat says that the half-life of fat in the adipose tissue is 600 days.  The half-life is the time it takes for the concentration of a substance to decrease by half.  So after 1 half-life, the concentration would have fallen to one-half of the original concentration; after 2 half-lives, the concentration would have fallen to one-quarter of the original concentration; after 3 half-lives, the concentration would have fallen to one-eighth of the original concentration; and so forth.

The half-life quoted by Dr. Peat was not explained in the study referenced by him, and so I followed the breadcrumbs to a paper by Hirsch and colleagues, which was luckily available (Hirsch, Farquhar, Ahrens, Peterson, & Stoffel, 1960).

Insulin's Role in Blood Glucose Regulation

"Insulin is important in the regulation of blood sugar, but its importance has been exaggerated because of the diabetes/insulin industry. Insulin itself has been found to account for only about 8% of the "insulin-like activity" of the blood, with potassium being probably the largest factor. There probably isn't any process in the body that doesn't potentially affect blood sugar.

When I initially read this quotation posted by one of Dr. Peat’s ardent followers on Facebook, it caught my attention because I was under the impression that insulin was the dominant factor in regulating blood glucose levels.

Normally, when blood levels increase, the beta-cells of the pancreatic islets secrete insulin into the bloodstream, where it binds to insulin receptors on organs and tissues throughout the body.  The adipose tissue, liver, and muscles are the principle sites that insulin exerts its actions on.  In effect, insulin is a storage hormone that rapidly clears nutrients out of the bloodstream.

(1) In the fat tissue, insulin suppresses the mobilization of fatty acids and promotes the synthesis of fatty acids and triglycerides.

(2) In the liver, insulin inhibits gluconeogenesis and glycogen breakdown and stimulates glucose oxidation and glycogen synthesis.

(3) In the muscles, insulin stimulates amino acid uptake and protein synthesis.

According to some of the most widely read physiology textbooks, in the absence of insulin all of the above processes become impaired, and fatty acids and amino acids are released in large amounts into the bloodstream from the fat tissue and muscles, respectively.  In the liver, these fatty acids are used to generate ketone bodies and the amino acids, substrates for gluconeogenesis, are used to generate glucose.  Because fatty acids flow to the liver at a high rate, and because insulin normally stimulates the use of ketone bodies by cells in the body, ketone bodies—namely acetone—accumulate in the bloodstream, thereby leading to acidosis, coma, and death.

Quick commentary on Dr. Lustig’s take on fructose

I’ve recently had the opportunity to skim through Dr. Robert Lustig’s book, Fat Chance.  I haven’t watched his YouTube lecture (and I don’t plan to), which people have used to justify the avoidance of fructose (and sugar) on, but I’m assuming that the main arguments in the lecture are summarized in his book.    I’m planning on addressing the entire book, bit by bit, but first, herein, I will provide commentary on each of Dr. Lustig’s conclusions about fructose, which can be found on pages 120 to 121.  Dr. Lustig’s comments are in red.

1. Triple the dose mean the liver needs triple the energy to metabolize this combo versus glucose alone, depleting the liver cell of adenosine triphosphate (or ATP, the vital chemical that conveys energy within cells).  ATP depletion leads to the generation of the waste product uric acid.  Uric acid causes gout and increases blood pressure.

This supposition was addressed briefly here.  

In short, there is no evidence that fructose, in the way that it’s consumed in the US now (i.e., with glucose), increases blood uric acid levels or causes gout.

Large doses of liquid fructose, unreflective of the consumption habits of the majority of the US population, does, in fact, raise uric acid levels, but this rise is only transient, no where near the levels seen in gout, and not necessarily harmful.

2. The fructose does not go to glycogen.  It goes straight to the mitochondria.  Excess acetyl-CoA if formed, exceeding the mitochondria’s ability to metabolize it.

Response to Dr. Paul Jaminet’s Rebuttal on Fructose

This rebuttal of sorts by Dr. Paul Jaminet was recently brought to my attention through a comment left on my Facebook page.  Danny Roddy was nice enough to lay out the arguments for me point by point.  Dr. Jaminet’s comments are in red.

1) “I think there’s substantial evidence that high fructose intake promotes endotoxemia” –PJ

This is not what I have found.

Diabetics and the obese have higher lipopolysaccharide (LPS) levels in their blood and they consume more fructose, primarily via HFCS, than people who are not diabetic or obese.   But as to specific food effects, the generation of LPS is buffered against on the ingestion of simple sugars because, for the most part, simple sugars are completely digested and absorbed in the upper part of the small intestines where microbial activity is minimal to non-existent. 

It is, however, conceivable that HFCS could lead to the generation of LPS because of the the presence of large starch molecules, if you recall.  Starch molecules, particularly when insufficiently cooked, can circumvent digestion and provide fodder for bacteria in the lower intestines, leading to the generation of LPS.

Endotoxemia occurs, though the definition is arbitrary, when blood levels of LPS rise by about 2- to 3-fold above normal levels.  Fats, in this regard, by permitting the passage of LPS into the body at high rates via newly made chylomicrons, execute the damages of LPS initiated by the increased proliferation of microbes in the intestines that was promoted by starches.

Are starches safe? Part 2

Part 1

(SEM image of corn-derived granule in blood after a serving of mueseli)

Previously on this blog, it was stated that starches and cereal grains were good food for cows and horses, but not man.  Man is instead better off eating food that is readily, easily, and perfectly digested.  Cases in point: fruit and fruit juices.  I will put forth herein why this is the case, and expand on some of the perils of excess starch consumption discussed in the last post.

                                               

A prominent feature of consuming starches concerns the previously discussed phenomenon called persorption (aka translocation).  Briefly, persorption describes the absorption of non-soluble microparticles through the intestinal lining and thereafter into the lymph vessels, mesenteric veins, and then distributed to tissues throughout the body.

Although persorption was known about since the mid 19^th century, the research on it has been sparse. (On my last search for articles on the topic in pubmed and medline, using the search terms “persorption” and “starch granule”, only five results were found.)

Nonetheless, there is still a lot we do know.  For one, we know that starch granules can appear, really, anywhere in the body, including the urine, cerebrospinal fluid, peritoneal fluid, fetal blood, umbilical cord, and milk of lactating mothers. 

Protective inhibition, energy generation, and the neuroprotective effects of ATP

Terminology

Axon: the slender part of a neuron that conducts electrical impulses away from the neuron’s cell body.
Autonomic ganglia: a cluster of neurons that provides a junction between the autonomic nerves originating from the brain and spinal cord, with those supplying tissues in the body.
Glial cells: non-neuronal cells that provide support to neurons by, for instance, producing myelin.
Heat shock proteins: “chaperone” proteins that, among their many other roles, help us resist stress (including heat stress).
Purine: a heterocyclic aromatic compound, consisting of a pyrimidine ring and an imidazole ring.  Examples include caffeine, adenosine, AMP, ADP, and ATP.
Protective inhibition: an organism’s response to overwhelming stimuli, manifesting as the cessation of metabolic activities.
________________________________________________________

Saturated fats, unsaturated fats, endotoxin, and implications of the Mani study

Recently, a study by Mani et al., was brought to my attention (Mani, Hollis, & Gabler, 2013).  Although I could only get my hands on the study’s abstract (the full paper is not available yet), in it, similar to the protocol followed by the studies referenced on this blog by Ghanim et al., pigs were fed 5 different oils, each given in porridge: coconut oil, olive oil, vegetable oil, fish oil, and cod liver oil.

Thereafter, blood samples were drawn from each pig at baseline, and at hours 1,2,3, and 5.  Surprisingly, changes in blood endotoxin concentrations were lowest in the pigs who received fish oil, and highest in those who received coconut oil; in fact, as much as 2-fold more, and in every sample analyzed.

As opposed to starch, any increase in blood endotoxin levels seen on the ingestion of fat is not likely due to an increase in bacterial proliferation and metabolic activities in the intestines.  Rather, it is more likely due to an increase in the transport of endotoxin from the intestines and into the body.  This is why results of the Mani study were surprising: For one, long-chain unsaturated fats stimulate chylomicron formation in the intestines, and this is one means by which endotoxin is taken into the body.  And two, unsaturated fats weaken the intestinal barrier, enhancing the incidental passage of substances like endotoxin into the body. 

Carbon dioxide, Glycation, and the Protective Effects of Fructose

Glycation processes and the potentially protective effects of an intensely active metabolic rate are topics that have been referenced on this blog frequently.  Glycation and cross-linking of molecules in the body contribute to the complications of diabetes and the changes in tissues seen in aging.  A salient consequence of these processes is the stiffening and loss of functioning of tissues in the body—including the skin, where a major substrate for glycation processes exists: collagen. 

Collagen is not only found in the skin, but also in the arteries, cartilage, and bones.  So, the health of the skin (its rigidness, degree of wrinkling, etc.) can serve as a (rough) barometer of the glycation processes that occur in the body. 

With age cross-linked proteins accumulate in tissues throughout the body.  This is a consequence of a few things.  For one, the turnover of proteins is decreased.  Two, the synthesis of proteins, despite the availability of amino acids, is, to some extent, impaired.  Three, fat is oxidized in preference to glucose, and as a result less carbon dioxide is produced and oxidative stress is promoted, thereby creating the conditions for high rates of AGE formation.  And four, energy production is diminished due to the cumulative damages incurred to mitochondrial respiratory protein complexes.

Stress, adaptation, and diabetes: an integrated picture (ABRIDGED VERSION)

A Canadian physiologist, Han Selye, advanced the research on stress and its physiological effects in the body in a series of studies in rats.   He found that chronic stress, regardless of the source, would produce characteristic changes in the body, and would, if prolonged, enlarge the adrenal cortices, atrophy the lymphatic organs, and ulcerate the lining of the stomach and duodenum (though, we know now that other organs are involved.)

Broadly stated, stress is ever present, so continual demands are placed on the body requiring ongoing adaptation to maintain physical and chemical balance, as well as the integrative functioning of its parts.  When this balance is disturbed, say, when stress is excessive or prolonged, the ability to adapt falters, fails, and, finally, pathology manifests.

In principle, these diseases of stress should be reversible, as long as the metabolic disturbances underlying them are eradicated, and oxygen and nutrients are supplied thereafter.  Thus, the exposure to stressors and disease can be conceived to exist on different points on the same continuum.  With regard to the interest of diseases, stress isn't the issue per se; rather, it is the body's ability to adapt to the stressors that it is continuously being exposed to.