Sunday, June 30, 2013

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.

Thursday, June 20, 2013

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.

Wednesday, June 19, 2013

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