I recently had this test as part of my blood work and have a level of 34, which is very low.  My doctor advised just as you have to start low and go slow watching how I feel.

This along with some other hormone supplementation has helped my overall well being and energy.  I can't remember when I had my last energy crash.  

As always, Thanks!

Interesting stuff, Dr Davis, regarding treating Lp(a) w/ DHEA.  

What are your thoughts on the efficacy of increasing/maintaining natural endogenous secretion via strength training and/or caloric restriction?

This is something I'm becoming more interested in as I creep closer to 40.

Hi, Mike--

I should have mentioned that I only suggest DHEA supplementation for these purposes in people age 40 and over.

Your idea of endogenous enhancement is the preferred, though relatively modest, route in younger people.

Thanks for reminding me.

I’m very interested in trying DHEA for this very reason. I’m am a 43 year old male in good health but who had very high cholesterol. I am currently using high strength fish oil and niacin along with cutting out most carbs from my diet. I have lost about 7 kilo since doing this and had some great plummets in my cholesterol. Problem is as I live in Australia we cannot get access to DHEA without paying obscene amounts of money via compounding pharmacies and doctor scripts as it’s a class 1 drug that is illegal. I know in the states you can get it as a nutritional supplement but Australia is backwards in this sense. Do you or any readers know of any sympathetic doctors who are interested in male health and would prescribe DHEA? It seems criminal that we cannot access the health benefits of this because of government bureaucracy.
Cheers from South Australia
Dave

Young people produce at least 12mg./day of DHEA; when we reach +/- age 30 our production of DHEA normally drops. I am led to believe that decline is +/- 2 mg./d. for every decade of our life past 30.

So, for an average patient of (say) 50 years supplementing daily with 10 mg. DHEA: the first 4 mg. is serves to "top up" the natural ageing deficit. The remaining 6 mg. is providing a 50% bonus level for the circulatory system to use thwarting Apo(a).

Sounds relatively safe intake. I'd like to hear if Apo(a)patients, who took it regularly in middle age, would be taking (say) +/- 15 mg. DHEA daily when they are in their 70's.

I am 58 years old and was recently tested and had levels of 4.510 ng/mL.  What levels do you recommend as targets for someone wishing to treat Lp(a)?

I have long been fascinated with DHEA but I read too many horror stories on Wikipedia and Consumerlabs.com about the dangers. Cancer, lowering of HDL, and aggressiveness are big turn offs. How do we balance these risks with the risk of heart disease?

-- Boris

http://curezone.com/forums/fm.asp?i=1448411#i

Problems with DHEA supplementation.

What do you think/know about magnesium oil's effect in raising levels of DHEA? I take oral magnesium in the form of Natural Calm (citrate i think) but three months ago I also started rubbing magnesium oil into my skin. I have read that this type of transdermal magnesium application raises DHEA levels. Any truth there, Dr.? Thanks

What is a good brand name DHEA, and can it be found in less than 50 mg tabs?

Thank you.

Anonymous,

I would recommend Life Extension brand of DHEA. I have had excellent results with Life Extension products over the years. They are a little more costly, but I believe the quality is top notch. Unfortunately however, the smallest dose of DHEA that LEF makes is 15mg.

Here is what Ray Sahelian, M.D. says about DHEA:

http://www.raysahelian.com/dhea.html

I myself had low levels of DHEA and low testosterone and I took DHEA (starting at 25mg and going all the way up to 75mg) and while my DHEA levels went up to the upper end of the reference range, my testosterone only increased by 9%-10%. I ended up discontinuing the DHEA because I couldn't get my testosterone levels up sufficiently and I was concerned about possible longer term side effects even though I didn't really experience any of the horror stories you read about online.

I don't have Lp(a) problems, but if I did, I would consider taking DHEA again in lower doses (15mg-25mg for me) however.

Hope this helps.

I've been taking the stuff since my mid-30s and found it to be great for general energy, mood and body composition. However, I've never been able to take more than 15 mg a day. That's low for a male, I know, but 25 or more and I get ferocious acne.

I was taking 10mg DHEA but have switched to 7-KETO (just 25mg a day at present). I believe that 7-KETO, as a naturally occurring metabolite reduces the risk of DHEA side effects, so was this a good idea?

(I am a 50-something female.)

Hi, Ben--

Sorry, no knowledge.

I did ask one of the manufacturers of topical magnesium preparations (creams, epsom salts) whether they had any data in humans showing effects on magnesium blood levels. They said they had not generated any nor were aware of any.


Several commenters--

The "horror stories" surrounding DHEA all refer to the higher, supraphysiologic doses I mentioned, not the low, physiologic replacement doses we use for Lp(a).

Also, this is about DHEA for Lp(a), not DHEA for youth preservation. Two different perspectives.

Q: I've been feeling really tired for a while now. My doctor checked my DHEA level which was very very low -- less than the level typical for an 80 yr. old woman and I am less than half of that! Could you please suggest some supplements for me? I know that there are DHEA supplements but these aren't available in Canada. Is there something else I can take? Thanks!





A: I have never been a fan of hormonal substitutes, including glandulars. With hormone replacements there is a great risk of atrophying the glands that normally produce the hormones. There are two reasons for this. One is a feedback mechanism in which if high hormone levels are perceived in the body the gland will be shut down to compensate. Secondly, glands are like muscles and must be worked to be kept healthy. Substituting for the glands makes them weak over time. I have seen some people claim that DHEA does not atrophy glands like other hormones, but rather leaves the adrenals producing the same level of hormones. Of course even if DHEA was not atrophying the glands and was leaving the glands to produce DHEA at the same level then the adrenals would still be producing at a diminished output. Therefore, the DHEA would do nothing to boost adrenal performance.



DHEA is classified as a weak androgen (male hormone). It is converted in to estrogen and testosterone, but not the balancing progesterone. This may lead to problems of elevated estrogen, including weight gain, thyroid dysfunction, problems with blood sugar, and problems with elevated testosterone, including increased body hair, and loss of scalp hair. There is also a lot of concern about the possibility of causing cancer or promoting existing cancers. There is not enough known about the actual long term effects of this hormone. Many of the studies on DHEA were done on rats, which do not have the same chemistry of humans. And the few human studies I have seen on DHEA were short term studies looking for improvement of certain symptoms, not side effects including the risk of adrenal atrophy. Overall I really think that DHEA supplements should be avoided!


DHEA is normally thought to decline due to age, though this is not necessarily the case. Primary production of DHEA occurs in the adrenal glands. Therefore adrenal function may directly affect DHEA levels. And the majority of the people are exposed daily to two of the biggest weakening factors for the adrenals, stress and stimulants. Stress can be physical, such as pain, or emotional. And both can be increased by reduced adrenal function since the adrenals produce the anti-inflammatories and anti-stress hormones for the body. Stimulants include caffeine, ephedrine, pseudoephedrine, and nicotine. Various pharmaceuticals can weaken adrenal function. The best known of these are steroids, such as Prednisone. Though anti-seizure medications, antifungals, cold medications, asthma medications, etc. can also cause adrenal weakness.


In short it is safer and more effective to build up your adrenal glands so they will produce their own DHEA at proper levels, rather than raising levels artificially to abnormally high levels. This is best addressed with vitamin C and pantothenic acid, the most important nutrients for proper adrenal function, and adaptogenic herbs. Adaptogenic herbs get their name from their ability to help people to adapt to stress by improving adrenal function.



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You have provided very nice information regarding testosterone supplements through your blog. Xenesis-T and Xenesis-EP for men and women a remedy for low Testosterone treatment, it will. It is the 100% natural supplement to overcome Testosterone problems.

At a dose of 50 mg daily, DHEA has not resulted in any decrease of HDL for me.

Adrenal genetic factors will not let everyone respond to "boosting". Of course, the same genetic quirks imply high dose DHEA (de-hydro-epi-andro-sterone)is not wise.

Worldwide +/- 1:1,000 develop late onset congenital adrenal hyper-plasia; among Hispanics 1.9%, Italians 0.3%, Slavs 1.6%,
Ashkenazi Jews 3.7% and caucasians generally 0.1%. Hirsutism (face hair) is an easy sign in women; adult acne for both genders.

A genetic enzyme 21-hydroxylase deficiency is the rate limiting factor in 95% of these cases. Then low amounts of cortisol are made. Signals for more, by cortico-tropins, "whips" the adrenal cortex; trying to get more cortisol output. But, the inability to synthesize cortisol makes all those building blocks go into production of androgens.

Additionally, there are 12 known genetic mutations of the gluco-dorticoid receptors. These make the body "resistant" to deal with the cortisol in circulation. Without de-activation (receptors a first step) into cortisone the cortisol level stays elevated.

In this situation both adrenals are, in a sense, overworking for no purpose. Progressively this leads to arterial hyper-tension down the way. So-called gluco-corticoid resistance, as a syndrome, develops in 10% of the elderly.

Point being that genetics, and the epigenetics of age, are some reasons why not everyone will respond to a "natural" plan. It also explains how different people respond to supplement dose of DHEA.

Paradoxically, genetics that mean patient can't be made to do what others can backs up Doc Davis' clinical DHEA use. If it is for combating high Lp(a) with small doses of DHEA.

I've never heard of topical magnesium supplements. It's awfully hard to imagine effective delivery of a cation/ionic salt through intact skin. Nor can I see any advantage in trying. Oral Magnesium supplements are readily absorbed and cheap. I'm also skeptical of claims that magnesium would optimize DHEA levels in most people. Magnesium is integral to the function of many enzymes, but unless it's the rate-limiting step in DHEA production and someone has a serious deficiency, I can't imagine how more magnesium would fix the issue. One CAN make a decent pharmacokinetic argument in favor of topical DHEA to minimize first-pass metabolism etc.

There's nothing like a warm bath with Epsom salt... I do believe magnesium is well absorbed through the skin, though I am ignorant of how it compares with oral supplementation. I get the same effects (deep sleep, vivid dreams) as with oral supplementation, only more pronounced with the bath.

My Lp(a) result was zero when I tested it a few years ago.

Was this inherited and will it likely always be absent? I can't find much if any info on nonexistent Lp(a).

I take 12.5 mg DHEA twice daily with no side effects - I just feel better. I am sure I was deficient - I plan on testing soon. I'm 43.

i tried 25mg and it drove me nuts. cut it down to 12.5mg and all of the crazy symptoms gone and i feel much better ocer all. wife tried 12.5mg and she felt bad. she cut it down to 6mg and she is fine too. thank you so much Dr. Davis

Thank you for your valuable post.  We have decided to share it with our global physician audience at PhysicianNexus.com:

http://physiciannexus.com/forum/topics/dhea-and-lpa
Jaerou Kim
Team Member
www.PhysicianNexus.com
Physicians Comparing Treatments Worldwide

Boris,

Based on 15 years of study and research, I would say (and truly without sarcasm) for you to stay away from Wikipedia (who get their info from google, FDA and American Medical Assoc) all of which are political agencies who DO NO ACTUAL RESEARCH THEMSELVES, but get their info from pharmacueitcal companies who HATE vitamins and nutritional supplements because they cannot patent them and make any money.

The horror stories that you have read at those sites are simply opinions of people who took as the gospel media soundbites on reported research and did not search out viable valid resources who study the actual research reports.

Dr. William Davis (of this site) is actually a very good resource for your valid health information.

Now stay away from those silly sites you cited and you can Live long and prosper.

Best of Health To You

Hmm, really?  So if I eat wheat (or was it 'carbs' generally?) and not enough animal fat, drink coffee, don't sleep enough, etc., Hashimoto's autoantibodies will start showing up in my blood?  And when I reverse the above, the antibodies will disappear and TSH, etc., will revert to normal?

Any support for this in the literature?

I suspect there needs to be some reeducation as to what is considered "normal" within the medical community as a whole. My TSH was last measured at 4.32, and is considered well within the range of normal, even though I've been complaining of hypothyroidism for a while now. Seems like we have to go into the doctor's office with steely determination to have these problems addressed.

Drs Davis and BG:
I think you are both on target with the attention you pay to hypothyroidism in relation to heart disease, and other related diseases such as obesity, diabetes, kidney and other hormone related problems.

Question please:
In your opinions:
1 Is the high incidence of hypothyroidism in the population throwing 'off' the lab  norms for TSH, FT3, FT4 or can we assume the numbers used by most labs are based on world wide or historical values?

2 Is 'Subclinical Hypothyroidism' real, or could it simply be a function of #1, or inadequate vitamin D3/iodine etc. I understand that 60% of the US population may be in that category.

Thank you
Mike V

You mention the connection between wheat and thyroid. If you want to read more about that, go to The Gluten File. www.theglutenfile.com There you will find a section on thyroid disease.

It is known that about 4-6% of those with Hashimoto's have celiac disease. I am sure that percentage would go even higher if one included those with non-celiac gluten sensitivity. There has been at least one study showing that thyroid antibodies disappear with the use of a gluten free diet.

Are there any studies showing wheat, vitamin D, etc. causing Hashimoto's? I suspect there isn't, but if population studies are looked into, perhaps you could find a correlation? Look at populations that generally don't consume much wheat, and see what their rates of Hashimoto's are. Or populations at upper latitudes vs those near the equator, and their rates of Hashimoto's.

However, if wheat, lack of sleep, poor diet, etc. does cause Hashimoto's, wouldn't it alter the male/female ratio of who gets the disease? Why would women still be more likely to contract Hashimoto's, if the cause is diet?

And in my case, several years ago I went to a low carb diet, restricted wheat, desserts consist of fruits/berries only, corrected my vitamin D levels, took fish oil, etc. I also tested negative for Celiac. Before these changes my thyroid tested normal (TSH in the low 1s). I was never overweight and exercised regularly too.

And this past month I was  diagnosed with Hashimoto's (high antibodies, TSH in the 3s, thyroid scan all lumpy). So... if there is a correlation, shouldn't my thyroid have improved, not gotten worse?

Bad_CRC,

I think you need to have the genetic susceptibility. On the animal pharm blog, I've listed a few that scientists have already correlated to Hashimoto's
--VDR polymorphs
--HLA polymorphs

I'm certain there will only be dozens others b/c these things (autoimmunity) don't happen alone.

Add'l, perhaps these things are also just signals for 'hibernation'...??  Perhaps we are only inducing ancient signals that are meant to protect and increase survival (low melatonin, high carbs, wheat/stress, fructose (from the Italian sodas I forgot to mention!), gaining weight, slowing down to Eat-Eat-Eat/stress, etc).

Any thoughts?

There are a few links in the literature regarding higher TSH, lower T3/T4 during winter months and lower vitamin D in the serum. Of course!

-G

G
I have no personal doubt that how well you choose your parents is of primary importance.
My late mother, and two brothers and sisters have all been  hypothyroid.
As in most diseases, I think other immune factors can be involved, some in the womb, some exposures in early childhood, while the immune system is still being 'programmed', others from bacterial or viral exposures.
It is said that vitamin D is quite important in a balanced immune system, but it starts very low in typical breast milk, and in very young children, and can remain low throughout life in much of the population.
Iodine deficiency was a critical factor in people not living near the coasts, until iodized salt was introduced in the early 20th century.
Lack of timely exposure to bright light is well known to "mess" with our biological clock, moods, and immunity.
I did not become aware that I was hypothyroid until my forties, and since have not found nutrition a major factor, until perhaps vitamin D.
With the exception of vitamin D, I have not personally been aware that other nutrition has affected my treatment.
Is there any co-relation between Hasimoto's, and other auto-immune conditions?

MikeV

Hello,

The question of gluten/wheat and autoimmune diseases including Hashimoto's is unquestionable and pretty in-disputable.

We just currently do not have the technology to fully detect this relationship.

(wait until we're a couple light years ahead...like Star Trek years/eons away)

JMC at the blog animal pharm has linked some fantastic resources from Loren Cordain and how the Paleo diet reverses autoimmune diseases (incl JMC's own rheumatoid arthritis).  Wheat is not the ONLY culprit. Legumes, Dairy/casein, nutr'l deficiencies, excessive fruit/HFCS, lack of exercise, lectins, etc are part of the equation for autoimmunity disorders as well.

Markers of potential coeliac disease in patients with Hashimoto's thyroiditis. Eur J Endocrinol. 2002 Apr;146(4):479-83.

OBJECTIVE: Coeliac disease (CD) is associated with autoimmune thyroid disease. Gluten sensitivity represents a spectrum, with at one end cases with severe gluten-dependent enteropathy, and at the other subjects with minor signs of deranged mucosal immune response. The aim of this paper was to look for signs of minor small bowel injury and immunohistochemical markers of gluten sensitivity in a group of patients with Hashimoto's disease. S
UBJECTS AND METHODS: Fourteen patients with Hashimoto's thyroiditis without serological evidence of CD underwent immunohistochemical analysis of jejunal biopsies.
RESULTS: In 6/14 cases (43%) an increased density of gammadelta T cell receptor bearing intra-epithelial lymphocytes was found. In 6/14 (43%) signs of mucosal T cell activation (presence of interleukin 2 (IL2) receptor (CD25) on lamina propria T cells and/or expression of human lymphocyte antigen (HLA)-DR molecules on crypt epithelial cells) were noted. In 4 out of 6 such cases (WOWO 80% of cases!!), HLA haplotypes were described in association with CD.
CONCLUSION: A significant proportion of patients with Hashimoto's thyroiditis present signs of 'potential' CD and of activated mucosal T cell immunity. The gluten dependence of such findings remains to be ascertained.  PMID: 11916614

Celiac disease and autoimmune thyroid disease.

Coeliac disease in patients with type 1 diabetes mellitus and auto-immune thyroid disorders.

Celiac disease-associated autoimmune endocrinopathies.

Endocrinological disorders and celiac disease.

Clinical review: Type 1 diabetes-associated autoimmunity: natural history, genetic associations, and screening.

Celiac disease and its link to type 1 diabetes mellitus.

Celiac disease in patients with an affected member, type 1 diabetes, iron-deficiency, or osteoporosis?

Gluten-sensitive enteropathy (celiac disease): more common than you think.




PROLACTIN:

There is HHEEEYYuge link betw man-boobs ('moobs' as know by 'experts' *ah* who have cup sizes that EXCEED mine). Prolactin grows mammary glands/breasts -- and this is induced by wheat, wheat, wheat/gluten, high carbs high carbs high carbs (lack of EPA DHA/vit D/vit A/etc).

Prolactin and autoimmunity.

Hyperprolactinemia and autoimmune diseases.

Prolactin in autoimmune diseases.

Prolactin in human systemic lupus erythematosus.

Prolactin and autoimmunity.

[Prolactin in the immunological system: synthesis and biological effects]

[Prolactin, a link between the neuroendocrine and immune systems. Role in the pathogenesis of rheumatic diseases]

Endocrine, paracrine and autocrine actions of prolactin on immune cells.


Hope that helps... so much understanding... but so little medical science... sometimes.



Mike V....TOTALLLY, I agree, in utero exposure determines our gene expression and is involved with epigenetics -- the genes in fact our future F1 F2 generations carry.  Epigenetics is supposed to enhance survival of our kind and adaptability... Personally, I think we are just de-evolving as the homo sapien race. Forget about the rain forests...look at us and our kids?

We are killing our future generations with the current low fat/whole grains food paradigm, lack of nutrient dense foods and high carb/high wheat/vit D deficiency/low fat guidelines in pregnant women.

Look at the rampant rate of death, mortality, chronic pain syndromes, heart disease, diabetes (OMG -- in CHILDREN), fatty liver (O-M-G.... in young YOUNG children), and the explosive degree of Hashimoto's and ALL autoimmune disorders (including AUTISM).  Some babies are even BORN with Hashimoto's thyroiditis.

What is going on?

For the first time in human history, our generation has high mortality/morbidity before their respective parents. (at least our parents had ample sunshine, their moms during gestation had saturated fats, EPA DHA, vitamin D and AEK, good nutrient dense food --though they might've poor; no air/water/land pollution, etc).


IMHO...That is just nuts... like our current world.
-G

Hello,

The question of gluten/wheat and autoimmune diseases including Hashimoto's is unquestionable and pretty in-disputable.

We just currently do not have the technology to fully detect this relationship.

(wait until we're a couple light years ahead...like Star Trek years/eons away)

JMC at the blog animal pharm has linked some fantastic resources from Loren Cordain and how the Paleo diet reverses autoimmune diseases (incl JMC's own rheumatoid arthritis).  Wheat is not the ONLY culprit. Legumes, Dairy/casein, nutr'l deficiencies, excessive fruit/HFCS, lack of exercise, lectins, etc are part of the equation for autoimmunity disorders as well.

Markers of potential coeliac disease in patients with Hashimoto's thyroiditis. Eur J Endocrinol. 2002 Apr;146(4):479-83.

OBJECTIVE: Coeliac disease (CD) is associated with autoimmune thyroid disease. Gluten sensitivity represents a spectrum, with at one end cases with severe gluten-dependent enteropathy, and at the other subjects with minor signs of deranged mucosal immune response. The aim of this paper was to look for signs of minor small bowel injury and immunohistochemical markers of gluten sensitivity in a group of patients with Hashimoto's disease. S
UBJECTS AND METHODS: Fourteen patients with Hashimoto's thyroiditis without serological evidence of CD underwent immunohistochemical analysis of jejunal biopsies.
RESULTS: In 6/14 cases (43%) an increased density of gammadelta T cell receptor bearing intra-epithelial lymphocytes was found. In 6/14 (43%) signs of mucosal T cell activation (presence of interleukin 2 (IL2) receptor (CD25) on lamina propria T cells and/or expression of human lymphocyte antigen (HLA)-DR molecules on crypt epithelial cells) were noted. In 4 out of 6 such cases (WOWO 80% of cases!!), HLA haplotypes were described in association with CD.
CONCLUSION: A significant proportion of patients with Hashimoto's thyroiditis present signs of 'potential' CD and of activated mucosal T cell immunity. The gluten dependence of such findings remains to be ascertained.  PMID: 11916614

Celiac disease and autoimmune thyroid disease.

Coeliac disease in patients with type 1 diabetes mellitus and auto-immune thyroid disorders.

Celiac disease-associated autoimmune endocrinopathies.

Endocrinological disorders and celiac disease.

Clinical review: Type 1 diabetes-associated autoimmunity: natural history, genetic associations, and screening.

Celiac disease and its link to type 1 diabetes mellitus.

Celiac disease in patients with an affected member, type 1 diabetes, iron-deficiency, or osteoporosis?

Gluten-sensitive enteropathy (celiac disease): more common than you think.




PROLACTIN:

There is HHEEEYYuge link betw man-boobs ('moobs' as know by 'experts' *ah* who have cup sizes that EXCEED mine). Prolactin grows mammary glands/breasts -- and this is induced by wheat, wheat, wheat/gluten, high carbs high carbs high carbs (lack of EPA DHA/vit D/vit A/etc).

Prolactin and autoimmunity.

Hyperprolactinemia and autoimmune diseases.

Prolactin in autoimmune diseases.

Prolactin in human systemic lupus erythematosus.

Prolactin and autoimmunity.

[Prolactin in the immunological system: synthesis and biological effects]

[Prolactin, a link between the neuroendocrine and immune systems. Role in the pathogenesis of rheumatic diseases]

Endocrine, paracrine and autocrine actions of prolactin on immune cells.


Hope that helps... so much understanding... but so little medical science... sometimes.



Mike V....TOTALLLY, I agree, in utero exposure determines our gene expression and is involved with epigenetics -- the genes in fact our future F1 F2 generations carry.  Epigenetics is supposed to enhance survival of our kind and adaptability... Personally, I think we are just de-evolving as the homo sapien race. Forget about the rain forests...look at us and our kids?

We are killing our future generations with the current low fat/whole grains food paradigm, lack of nutrient dense foods and high carb/high wheat/vit D deficiency/low fat guidelines in pregnant women.

Look at the rampant rate of death, mortality, chronic pain syndromes, heart disease, diabetes (OMG -- in CHILDREN), fatty liver (O-M-G.... in young YOUNG children), and the explosive degree of Hashimoto's and ALL autoimmune disorders (including AUTISM).  Some babies are even BORN with Hashimoto's thyroiditis.

What is going on?

For the first time in human history, our generation has high mortality/morbidity before their respective parents. (at least our parents had ample sunshine, their moms during gestation had saturated fats, EPA DHA, vitamin D and AEK, good nutrient dense food --though they might've poor; no air/water/land pollution, etc).


IMHO...That is just nuts... like our current world.
-G

Mike V--

The newest data, e.g., the HUNT Study, are analyses of events based on TSH. It therefore factors out the effect of population distributions.

You are correct, however, in pointing out that previous analyses were flawed precisely for this reason.

As usual thanks to all for the education, and for all you do to penetrate the blood brain barrier between the specialties, Big Medica, and us (the great 'unwashed'. )

MikeV

Hi Doc,
We are seeing a very high % of our patients with zinc deficiency - similar to the whole vitamin D thing. Just wanted to share this with you since zinc is also correlated to blood sugar and cholesterol problems. Would love to see what you find in your patients with regard to this nutrient as well.
Regards,
Pat Elliott ND
www.elliotthealthcare.com

Pat Elliott  --

How do you define a zinc deficiency? I've read that serum zinc is pretty inaccurate (as is copper or magnesium serum testing).

Looking at other biomarkers, or a zinc taste test?

I'm guessing that when "Nameless" took up the low-carb eating plan, they may have also increased eating soy.  Soy can really mess up the hormones.  I think we can blame soy for all this thyroid trouble and fibromyalgia and fatigue related troubles.  Add to that inadequate fish oils, butter, after years of telling us to avoid fats and sunlight (vitamin D) and you get a nice picture of what has happened to far too many of us.

I know this is an old post but I'm just going through all the thyroid-related posts. My TSH got flagged at a 9 when I went for a physical a couple weeks ago, and further tests came back with a Hashimoto's diagnosis.

I just don't know. I follow a gluten-free diet, in fact I avoid all grains. I avoid all sugars, I don't consume any high-PUFA vegetables oils. I have not eaten any sort of soy (except for rare splashes of fermented soy sauce here or there) in a dozen years. I always cook any veggies I might eat  that call into the goitrogenic category. I supplement with 5000 IU of D3 in gelcap format daily. I consume most of my fats as sat fats/animal fats. I take fish oil, cod liver oil. I love to eat sardines.

Yet my thyroid apparently has slowly been getting worse over the last couple years. My TSH is definitely higher than it was in 2007, and that was higher than it was in 2006 - slowly been climbing over the last few years until finally the doctor red-flagged it.

I have Hashimotos. Was diagnosed at 15. Had it long before then. I am convinced it is genetic when I look at other family members (although no-one else has been diagnosed). I am on 'correct' dosage of thyroid hormones but many of the symptoms still exist and I would LOVE to blame my GP but the fact is that they are overworked and are doing the best with what they have - like the rest of the population. Recently diagnosed with anxiety by a psychologist. Does this cover the hashimotos symptoms completely or partially? Who knows? All I know is that I am drunk now as I am bone tired from trying and failing from everything from relationships to work - alcohol seems to be the only way out...although my psychologist has told me it isn't - just being tired and weak I guess. I'm sure you will delete this post as soon as you see it blog owner, but before you do, I hope a few Hashimotos/anxiety sufferers see one person struggling to be better despite the messy interference of life. Having a temporary failure right now but will be back on the horse again tomorrow like every other day.

Love you all.

XXX.

JMC at the blog animal pharm has linked some fantastic resources from Loren Cordain and how the Paleo diet reverses autoimmune diseases (incl JMC's own rheumatoid arthritis). Wheat is not the ONLY culprit. Legumes, Dairy/casein, nutr'l deficiencies, excessive fruit/HFCS, lack of exercise, lectins, etc are part of the equation for autoimmunity disorders as well.

What a brilliant idea! Thanks for sharing this information. I have hypothyroidism for almost 4 years and it was terrible. I am currently taking porcine thyroid .  Now I'm gaining back my normal life.

I don't know how individuals with mis-sense SNP for gluco-kinase regulatory protein (ex: GCKR rs780094) fit into the pattern. They get more liver steatosis (fat build up) with attendant elevated LDL and triglycerides, despite less fasting glucose and less fasting insulin numbers; while their 2 hour blood glucose runs high (GCK gene is very determinate of 2 hour glucose levels), showing down-regulation of the homeostatic model for Beta cell function (HOMA-B).

Normally GCKR regulates triglycerides and determines persons glycemic traits by governing how glucose is stored and how it is dispersed. GCKR also geneticly regulates the availablility of substrate used for de-novo lipo-genesis.

Gene SNP of protein phosphatase 1regulatory (inhibitor) subunit 3 B (PP1R3B rs4240624) manifests increased liver steatosis  and both elevated LDL and elevated HDL; with low fasting glucose. PPP1R3B codes for controling protein and modulates the break down of glycogen (storage glucose moleccule).

Together PPP1R3B and GCKR are integral to blood sugar dynamics and the levels of lipids in circulation.

If Doc's regimen counter-balances individual missense genetic workings, like those above, then that is impressive corrrection achieved through intervention . I presume for people with liver steatosis missense mutations (ie:  SNPs like above) elevated LDL treatment using statins would be bad for their liver.

Statins might be helpful if you have bacterial pneumonia:
http://www.bmj.com/content/342/bmj.d1907.extract?sid=f762e55c-1a0b-4ef3-81c4-f31cc472a372

That's because the rapidly growing pneumococcal bacteria are very susceptible to HMG-CoA reductase inhibitors (statins). The bacteria have similar cholesterol compounds (hopanoids) in their membranes, essential for their membrane function. With the statins blocking the hopanoids, they die....very quickly.

All bacteria have a mevalonate pathway.  The HMG-CoA reductase enzyme is inhibited in bacteria and are VERY toxic to bacteria. So thus, you have a "statin-benefit" because it kills the bacteria, before it kills or injures the patient.

Statins can essentially inhibit biological life forms.
Dr. John

HI, Might--

As usual, you've come out of left field with a totally unexpected issue!

I'm not sure how this genetic variant fits into this argument. It is, to my knowledge, a very rare diagnosis.

I don't envy Doc trying to sort out who needs what treatment. Genetic high cholesterol entails over 50 amino acid variations out the jumble of 692 amino acids assembled into relevant complexes.

Pro-protein convertase subtilisin/kexin-9 (PCSK9)is involved in familiar hyper-cholestemia. Those who make too much PCSK9 (in the liver and small intestine) rapidly degrade their cholesterol receptors and can't pluck much LDL out of circulation; plasma cholesterol rises.

Should one's genetics foster making too little PCSK9, then cholesterol receptors don't degrade. This promptly shunts cholesterol into the liver lysosome (an organelle inside a cell)for break down; thus they  measure low cholesterol in the blood.

I speculate Doc's diet, in "normal" genetic people up-regulates cholesterol reception. Which means his program has the epigenetic effect (from diet dynamics) on "normal" liver/small intestine genes in a way that less PCSK9 is expressed

The caucasian anglo-saxon PCSK9 D374Y mutation causes 4 times the normal cholesterol in patients. Their risk factor for pre-mature death is 10 years earlier than even more benign PCSK9 mutations; so Detective Doc Davis is willing to prescribe statins for people like them.

I might be one of these poor souls.

Eating a strict diet, one Dr Davis would be very proud of... I'm lean as can be, feel great, but my cholesterol shot through roof (while HDL dropped).    

Hi Annon.,
Internet self-diagnosing shouldn't replace a good medical consultant. My comments are not qualified medical assesments; am a layman.  

My favorite cousin has had her cholesterol testing well over 300for several decades, and is now in her late 70s. Like Doc chided me earlier, there are "genetic variant" being "very rare diagnosis."

What do you think about KIF6?   I was tested and found to be a non-carrier, and I was subsequently told that statins would likely not benefit me as much as diet/lifestyle changes (I'm ApoE 3/4 as well).  Does that also mean that niacin would not help?

To say the least, I am very disappointed in Dr. Davis' stance regarding ApoE 4 & statins. There is abundant evidence suggesting statins are counterproductive to brain health, which is much more pronounced in Apo E4's who are already at high risk for alzheimers disease. It isn't only about lipids, there is a larger picture to consider. The brain requires cholesterol.  Also, high cholesterol levels are associated with longevity in the elderly.

Alzheimers and the relationship of ApoE4 is different than other ApoE isoforms (like ApoE 2 & 3). In normal people ApoE is integral to clearing amyloid Beta from the brain; it forms a conjugate (ApoE/AmyloidB)that is moved out across the brain blood barrier by LRP-1 (lipo-protein related protein 1).

ApoE4 is acted upon (cleaved) in brain neurons, yielding rump fragments with unique Carbon- terminals; and,  ApoE4 degrades easier than ApoE 2 &/or 3. These ApoE4 fragments, when in a brain cell's cytosol, influence that cell's mitochondria hydro-phobic pattern of lipid binding.

The ApoE4 fragment properties  do 2 unwanted things to the brain cell mitochondria. It decreases the mitochondria ability to perform tasks involved in glycolysis (glucose energy). And is antagonistic to PPAR gamma; PPAR gamma is what would otherwise promote adequate mitochondria bio-genesis.

ALzheimer lesions show higher amounts when measured in individuals with concurrent Type II diabetes and the ApoE4 isoform. The ratio of insulin in the cerebro-spinal fluid to the amount of insulin in the blood also shows a difference depending on the specific ApoE geno-type.

Alzheimer brains are using less glucose; patients show less receptors for insulin-like growth factor and insulin, as well as less insulin degrading enzymes. It is postulated that depending on the individual's ApoE variation there is a different amyloid Beta response to brain insulin.

Normally one goes from glucose intolerance to hyperglycemia and then elevated insulin circulating as become diabetic. Yet experiments show that giving insulin improves diabetic neuro-pathy in the brain; it seems to be a way peripheral insulin resistance causes different tissues to respond.

In Alzheimer experiments with supplemental insulin (nasal, etc.)administration cognitive function improved. This response was more significant in those with the ApoE4 allele (compared to other ApoE types with Alzheimers, who also improved cognition ).

So, the Alzheimer enigma seems to involve energy format dynamics for ApoE isoforms more than specific levels of cholesterol. This is not a comment on ApoE homo-zygote genes relationship to cardio-vascular risk factors, or brain lipid metabolism.

Mito
You sound like Suzanne Craft.  I like her work.

You make an excellent point here:

...eat more healthy whole grains" diet that introduces grotesque distortions into metabolism

We are encouraged by transient sources that this is almost always the best alternative for other fattening foods, yet people never really delve deep into the cons of this transition either.  It truly does take dedication to be well-informed about the dietary changes you make in your lifestyle.

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I had a body scan a few years ago, and my plaque count was 1050, when they told me that 150 was considered high, I thought  I would implode at any moment, I went to a lot of different cardiologists and had all kinds of tests and they said to exercise and not  worry about the plaque. One Dr. put me on lipitor and 3 days later I could hardly walk from the muscle pain, he told me to stop taking it and I tried niacin and red rice with the same results. I don't know how to reduce the plaque, the Dr's all said it was hereditary . I am open to any advice.

Hi, Anne--

Note that this is the blog that accompanies the Track Your Plaque program that focuses on just this issue. It means 1) identify all causes of plaque, then 2) correct them, preferably using natural means.

Dr. Davis,
I don't know if you have already addressed this topic in prior posts but allow me to suggest that in lieu of consuming statin drugs, even for the aforementioned outliers, it is possible to achieve reduced LDL cholesterol and increased HDL cholesterol by supplementing with magnesium.
(All the ensuing statements below I humbly attribute to Mildred S. Seelig and Andrea Rosanoff, "The Magnesium Factor," pages 139-147.)
1. Statins (Lipitor, Zocor, Baycol, Mevacor, etc.) are designed to lower cholesterol by inhibiting HMG-CoA reductase, which is the enzyme responsible for the synthesis of cholesterol.
2. These drugs when studied, not only lower cholesterol, but also reduce total mortality, cardiac mortality, the total incidence of heart attacks, angina, and other non-fatal cardiac events. (p.140.)
3. They also made the blood platelets less sticky, they slowed the progression of plaques and stabilized them, and they reduced inflammation in the blood vessel tissue. (ibid.)
All these results, and more, Seelig further informs the reader, are a result of reduced mevalonate in the cells, which is the direct result of an inhibited HMG-CoA reductase, which is the enzyme that statins are designed to inhibit.
Now stay with me for a second because here is where it gets interesting.
4. Magnesium is a natural inhibitor of HMG-CoA reductase. Here magnesium and statins are comparable (p. 141.)
5. Magnesium also acts on two enzymes, phosphatase reductase and phosphohydrolase which reactivate HMG-CoA reductase. By its effects on these enzymes, which contrast one another, magnesium can either stop cholesterol formation or allow it to continue depending on the body's needs.
6. Magnesium also activates another enzyme, lecithin cholesterol acyltransferase (LCAT) which, through this action, converts LDL cholesterol to HDL cholesterol -- increasing HDL and reducing LDL.  (Statins cannot do this.)
In the interest of brevity, I'll conclude by saying that whereas statins are known to reduce cholesterol and perhaps achieve other cardiovascular benefits, this is due in large part to their suppression of mevalonate, brought about by their inhibition of HMG-CoA reductase.
In contrast, magnesium not only inhibits HMG-CoA reductase, meaning that it would achieve the same results as statins in "1, 2, and 3 above," but it also converts LDL cholesterol to HDL cholesterol, achieved by its activation of LCAT, which is something that statins do less consistently.
Further, instead of poisoning HMG-CoA reductase as statins do, magnesium inhibits it in ways that can be reactivated by other (magnesium dependent) enzymes so that the body can naturally make the mevalonate and cholesterol it needs.
This is important because vitamin D is synthesized from cholesterol (when using the sun's rays), and cholesterol is also the precursor to testosterone, estrogen, and other steroids.
So I encourage you to consider using Magnesium for those Apo-B cases that cannot be addressed by carbohydrate restricted diets.

Sorry, meant to say Apo-E cases.

[...] sensitive to dietary fat, particularly saturated fat, as well as carbohydrate. William Davis MD has found that for these individuals, moderation of both fat and carbs is necessary to avoid elevations in [...]