Biotin and High Protein Diets

This is a follow up to my previous post about the Dukan Diet and Vitamin A.

There is a new fad which is an off shoot of the Paleo diet.  It’s an all meat diet.  I had heard of it over a year ago before it was popular; I read much on this website: http://www.zerocarbzen.com.  I tried it.  It didn’t work for me.  There are stories of miraculous transformations, unicorns, and mermaids resulting from this diet, so it made me really disappointed that it didn’t work for me.

I mean, that website called it the “Original Human Diet.”  So, am I less than human since it didn’t work for me? No. (I’m sure it was just that old party line about adaptation and electrolytes….right……).

Now, it has been trumpeted all over the internet by Shawn Baker, M.D., through his instagram account, instagram.com/shawnbaker1967.   People are actually supposed to eat like lions!  (Because look how similar we appear….right?).

I did ask him through instagram – What about people with ornithine transcarbamylase (OTC) deficiency?

His response was it was a rare disorder.  Not true.  It is the most common ureagenesis disorder with a prevalence of 1 in every 40,000 (https://adc.bmj.com/content/84/1/84)

Sometimes it is detected at birth and sometimes it is not detected until adulthood, when one tries to eat the “Original Human Diet” (only meat!  we’re supposed to eat like the lions remember?  sharpen your nails/fangs!).

When I last posted about OTC deficiency, I had left off with the bit about biotin possibly playing a role.

Remember that OTC deficiency is a urea cycle disorder.  Urea comes from ammonia which comes from meat (or any source of nitrogen).  Ammonia is turned into urea and excreted from the body.  If the ammonia cannot be turned into urea and excreted, then ammonia builds up in the body.  It is toxic for humans when reaching high enough levels (when you eat enough meat from which it comes or take certain medication), and death and/or brain damage may be the result.  You can look up ammonia online and research its toxicity for humans if you don’t believe me.  So, anything that interferes with OTC enzymes results in an increase in ammonia in the human body.

OTC deficiency is listed as a genetic disorder.  But in the last post I presented evidence of others’ research that may dispute this.  OTC deficiency can be the result of Vitamin A deficiency.  And it can be the result of biotin deficiency.

An experiment in 1996 through Osaka University Medical School in Japan found that rats who were made biotin-deficient for 6 weeks had a significantly higher plasma ammonia level than the control group of rats who were biotin-supplemented.  ‘OTC gene expression in the liver of BD rats was 40% lower than in BS rats…These data suggest that biotin deficiency decreases OTC activity and the amount of OTC mRNA.” To clarify, BD=biotin deficiency, BS=biotin supplemented.  So this shows a clear effect of decreased biotin on OTC enzymes, necessary for ammonia/urea metabolism.  You may also soon see recommendations for pregnant women to eat more biotin-containing foods, because it extremely important for fetal development, recent research shows.  But this is not widely known information yet.

In addition to rat studies, there is one human case study.  I must highly commend the doctors in this case.  They had a patient with ammonia levels that would not drop to normal using the typical treatment of arginine/lactulose/citrulline and low protein diet.  This patient had many disorders, mental and physical.  His ammonia level was 120mg (reference range of 12-47mg), and even after the treatment above, was still fluctuating between 120mg and 226mg.  This is very dangerous because of the potential for brain swelling and death.  A really smart & savvy doctor began treating him with 800mcg of biotin daily and the patient’s ammonia level fell to 69mg.  Amazing.  The patient had normal liver function tests, which means the hyperammonia was due to an OTC deficiency.  Abnormal livers also have problems processing ammonia into urea and if this patient’s liver panels were abnormal, that would have been the likely diagnosis and not OTC deficiency.  So, we now have a valid medical case proving that OTC deficiency can be corrected by biotin supplementation.  All of the sudden ammonia levels decrease as a result of biotin.  Is it truly a genetic disorder?  Or is it an environmental disorder due to lack of biotin? If you would like to read the case study, it is “The Effect of Biotin on Human Ornithine Transcarbamylase Deficiency Diagnosed in Late Adulthood” by Alan Scott Sacerdote, Gul Bahtiyar, Grazyna Kaluta, Judith Giunta, Taiga Inoue, George Ezeji, and Annpia Baby.  It was presented March 7, 2015 at the Endocrine Society’s 97th Annual Meeting and Expo in San Diego, California.  Presentation Number SAT-476.

The fact that both vitamin A and biotin deficiencies can cause OTC enzyme deficiency leads me to believe that this “genetic disorder” is actually a “genetic adaptation” by humans who evolved eating much vitamin A and biotin in their diets.

And to further explain, it has already been proven by the American Chemical Society that any increase in protein in the diet necessitates an increase in vitamin A.  This is because vitamin A is depleted from the liver by excess protein.  Protein eaten in the diet can become retinol binding protein, which brings vitamin A from the liver to the tissues.  The vitamin A that is taken from the liver must be repleted.

Liver contains the most concentrated amounts of both vitamin A and biotin.  And it is so seldom eaten (if at all) on a high protein diet.  But every culture that ate animals ate organ meats as well.  And this may be the missing piece to prevent failure on an all meat diet.

I wish the doctors would have also tried giving their patient vitamin A, just in the interest of science to see if it would decrease the ammonia level.

I really do want to know why, what, how it is caused.  What is the natural human diet.

 

 

 

 

 

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Leisure is

Leisure is a luxury
only when alone
breath can be released
the pins can be removed
and you begin to heal
slowly.

Keeping up the Charade

To succeed in life, it is essential to understand that what matters is not how things actually are, but how they seem.  A master of life is a charmer who can appear to be whatever is needed at the moment.  Remember that everyone wants to be charmed and no one wants to know the truth.  The only place where the truth is actually sought after is a court of law.  The masses believe what they hear.

Remember that success depends on the good favor of those above you, especially in a feudal society such as the United States of America, where power is in the concentrated hands of the few.  Just because the few are powerful does not mean they are good or smart.  But remember never to insult them; your ensured success depends upon the favor of these imbeciles.  Remember this.  You must remember this.  Your life depends on it.

So, to be a good actor (charmer), you must suppress your feelings of frustration with this reality.  Only confide in privacy or not at all.  If a friend wants to talk, tell them to call you.  Don’t talk in public.  If you can’t control your mouth, stick something in it.

It’s difficult not to complain when all of your life is frustrating, but try not to.  Everyone will repeat whatever you tell them, and as they say on TV, it can and will be held against you.  Remember this.  You must be a pretty Pollyanna and then, maybe then, the feudal lords will look down on you with favor and you may succeed in exiting the asylum through your success.

Good luck.

 

 

 

 

Hypoglycemia: The effects of Glucagon and Vitamin A

Hypoglycemia: It’s Symptoms and Causes

One infrequently discussed problem of low carbohydrate diets is hypoglycemia symptoms.  If you’ve never had hypoglycemia, be glad.  The word hypoglycemia means “low” (hypo) “sugar” (glyc) “in blood” (emia) – Low blood sugar. The symptoms include sweating, shakiness, dizziness, irritability, cold extremities, lightheadedness, anxiety, and many others.  There is reactive hypoglycemia, which occurs shortly after eating a meal that stimulates excess insulin release leading to low blood sugar and its accompanying symptoms.  (I want to point out here that hypoglycemia should be determined based on overall symptoms and not the blood sugar level itself.  If someone is used to a perpetually high blood sugar level and then it goes to normal, that person will have hypoglycemia symptoms even thought they don’t “technically” have low blood sugar).  Insulin release can be caused by foods with a high glycemic index (those that are quickly converted into glucose) or a food sensitivity to whatever was ingested.  Although the food sensitivity cause of hypoglycemia is hardly ever discussed in modern medicine, it is a fact and has been documented in historic medical literature.

In this model of hypoglycemia, the cause is excess insulin driving blood sugar down too low.  Insulin takes the blame for a lot, but in order to truly understand this, we need to look at all sides of this equation.

Glucagon: Its Role and Importance

Insulin drives down blood sugar so that the blood sugar does not get too high.  Glucagon has the opposite effect – it releases stored blood sugar from the liver and muscles during fasting.  There are cells that simply must have glucose in order to survive.  Red blood cells need glucose.  The brain needs glucose.  Because of how essential to life it is, we have the hormone glucagon to provide us glucose when we cannot get it from the environment.

So on the other hand, hypoglycemia during fasting can be a result of dysfunctional glucagon.

The Unacknowledged Importance of Vitamin A in Fuel Regulation and Hypoglycemia

Vitamin A makes an appearance here because it is essential to optimal function of both insulin and glucagon.

Vitamin A is essential on a low carbohydrate diet because the alpha cells of the pancreas cannot secret enough glucagon without it.  This comes from a 1994 study titled “Effects of vitamin A deficiency and repletion on rat glucagon secretion.” (Pancreas. 1994 Jul; 9(4): 475-84.  PMID: 7937697).  In this study it was found that “glucagon secretion was markedly impaired in islets and pancreases of vitamin A-deficient rats or rats that had at some time been cycled through vitamin A deficiency (ever A-def) despite repletion with retinoids for 2-4 weeks.”  Insulin secretion by beta cells was also impaired (the insulin secretion impairment has been confirmed many times since due to the obsession with insulin; no one cares about glucagon to research it enough). The researchers also found that this glucagon secretion impairment appeared early in the course of the vitamin A deficiency.   So, in my opinion, hypoglycemia due to glucagon secretion impairment is the first sign of vitamin A deficiency, not problems with night vision, which is the cartoon-version of vitamin A deficiency in every lay person’s vitamin book.

Even when glucagon is functioning optimally, if one is on a low carbohydrate diet, the glucose release from glucagon cannot be the sole fuel of the body.  There simply isn’t enough to power the whole body on the little amount of glucose that the body secretes from insulin.  If you don’t have an alternate fuel source to rely on, you will be dependent on that little supply of glucose and feel pretty impaired.  Remember, you are cutting carbohydrates on a low carbohydrate diet and your two other fuel sources are protein and fat; neither can supply much glucose.  But the body can use fat for fuel.

But again, vitamin A steps in.  The body can’t use fat for fuel effectively without vitamin A.  When vitamin A is deficient, urea cycle enzymes are increased.  The urea cycle is the process of metabolizing protein, not fat.  The theory is that without vitamin A, the fuel to be relied on will switch to protein (a source of glucose) and not fat. (“Vitamin A deficiency increases protein catabolism and induces urea cycle enzymes in rats.” J. Nutr. 2010 Apr; 140(4): 792-8. PMID: 20181784).  Then you are back to relying on glucose on a low carbohydrate diet,  the need of which can never be met due to the insignificant amount of carbohydrates.  To be successful on a low carbohydrate diet, you must be able to metabolize and use fat.

Summing up

To conclude, if one is suffering from hypoglycemia on a low carbohydrate diet, the most likely cause is vitamin A deficiency.  The secretion of glucagon in meeting the minimum glucose requirements of the body is dependent on sufficient vitamin A.  And the effectiveness of the body in switching its fuel source to fat instead of continuing to rely on glucose through the urea-protein cycle is also dependent on vitamin A.  The first symptom of vitamin A deficiency is hypoglycemia.

 

 

 

 

 

 

 

The Dukan Diet & Vitamin A Deficiency

This is an old news story but I like to investigate what goes wrong on low carb diets.  So many people think extreme low carb diets are infallible and everyone should be able to do them.

A UK newspaper, the Telegraph, reported in 2012 the case of a man who almost died while on the Dukan diet, a low carb diet created by French MD Pierre Dukan. (http://www.telegraph.co.uk/lifestyle/wellbeing/diet/9013566/The-man-who-nearly-died-on-the-Dukan-diet.html)

After two days on the “Attack” phase of the diet, which consists of only protein, Ashley Harrison was in the hospital in a coma with encephalopathy (brain dysfunction).  In the article, the encephalopathy is attributed to ammonia poisoning.  Ammonia is the by-product of protein metabolism in the body and can cause brain swelling.

It happened that Mr. Harrison had a genetic mutation resulting in a deficiency of ornithine transcarbamoylase (OTC)

Ammonia and OTC are part of the urea cycle.  While genetics may play a part, it is possible this man had a Vitamin A deficiency and that this either contributed to or was the real cause of his ornithine transcarbamoylase deficiency.

According to researchers, “Activities of hepatic carbamoylphosphate synthase-1 (CPS-1) and ornithine transcarbamoylase (OTC) were significantly lower in vitamin A – deficient animals than in control rats at the end of 13 weeks of feeding.  While the liver levels of ornithine and polyamines were significantly greater, that of glutamine was lower in vitamin A-deficient rats than in pair-fed controls.  The results suggest that vitamin A deficiency leads to a reduced efficiency of urea synthesis pathway, thus accounting for the increased ammonium nitrogen (Am-N) excretion seen in vitamin-A deficiency.” J. Nutr. 1989 Jan. 119 (1) 29-35.

Did his doctors know that vitamin A deficiency can cause OTC deficiency?  I bet my next paycheck they don’t have a clue.  Did they even check his serum vitamin A level?  No way Jose.  Did this man have a vitamin A deficiency that lead to his OTC deficiency?  This was a lost scientific opportunity and now the world will never know.

Part II: Did biotin deficiency lead to this man’s ornithine transcarbamoylase deficiency?  It certainly could…

McMedicine, Subclinical Iron Deficiency and Copper Deficiency

Iron and Copper deficiencies are widespread in the modern world.

Because we are told to cut down on foods that contain saturated fat (and therefore, iron and copper), much of the western world has subclinical iron and copper deficiency.  I will have to edit this post later; for now it is a collection of my thoughts.

Serum levels are turning out to be extremely unreliable indicators of nutrient status.  What seems to happen is that tissue levels of nutrients will be deficient, but serum levels will read normal.  And there are no doctors who biopsy tissue for lab tests of nutrients.  The only tests that doctors run are blood work.  And if everything in blood work appears “normal” well, then, it must all be in your head.  Below are some serum levels that are false positives of nutrient status (references to follow later).

-Serum Vitamin A – found to be normal while the tissue levels are deficient, especially in obsese individuals.  Vitamin A has a major role in adipose tissue which is being studied with conflicting results.

-Folate/folic acid – found to be normal while the cerebral spinal fluid (CSF) is deficient in active methyltetrahydrofolate (MTHF).  Also falsely positive because of the large intake of folic acid, the inactive/unnatural form of folate that a lot of people cannot convert to active folate.  Active folate levels are not measured (not sure if they can be measured in blood…must research this)

-Copper – copper levels will be normal in blood while copper-dependent enzymes such as ceruloplasmin and superoxide dismutase will be deficient.

Iron and copper are important to brain health, but this is largely ignored by pretty much everyone.  Here I will have to compile my research, but I have read that iron is especially important for creating neurotransmitters.  I hadn’t heard that before.  A deficiency in iron is noted as a cause for behavioral disturbances such as symptoms associated with attention deficit disorder and autism spectrum (Hematol Oncol Clin North Am. 1987 Sep; 1 (3):449-64.).  It can even cause such disturbances when clinical anemia is not present.  You can have low or mid-normal serum iron and not have enough tissue iron – such as in your brain or muscles – and it can affect you without causing anemia.  I suspect that anemia would not appear due to the blood receiving stored iron from the liver.  The liver has large stores of iron.

Will edit later…

 

I revealed something I shouldn’t have.  Again.

I have a compulsion.  I want to tell.  This urgency to fill the silence, to connect in words.

It’s not to create illness or spread gossip.  I want to reveal and tell because that is the only intimacy I have; I am so void of connections.

And humans need intimacy.  Not just sex.  Sex is boring.  The soul’s intimacy is revelations embraced.  Sometimes, I do feel this even when I am quiet.  It is so rare!  I can only count on one hand the times I have felt such content in silence, such peace.  It was at least two years ago when I had felt this way.  It was a sunny day and I was walking in a parking lot and I suddenly felt so at peace and that I truly needed nothing more except to exist in this.  And the worry and persistent low level annoyance with living was gone.  And it occurred to me that I was happy.

I wish I could live in that moment every day.  Sometimes I try to figure it out – maybe I ate the right thing that day or did something different.  I was trying a different diet at the time but it later caused problems (waking at 3 a.m. feeling anxious – I always slept the whole night without any anxiety).  But most days are full of fear and various symptoms of malingering illness which there is no help for.

My deepest desire is intimacy.  But I feel like I am truly intimate with no one.