Sunday, March 24, 2013

Ancient Transporters: HDL and LDL Lipoproteins Carry Precious Cargo




The NCEP/ATP III Cholesterol Guidelines Bogus: 'Cholesterol Limits Lose Their Lustre'

Conventional medicine at this time uses Big Pharma-funded assessment and treatment guidelines which promote the use of statins as first line in order to 'treat' the LDL (goal less than 70, 100, or 130 mg/dl) to targets based on risk stratification, e.g. age, prior family history coronary events, low HDL, smoking and presence of hypertension.

What are the true root causes of these 'risk factors' in light of evolution (if you believe in evo)? Is LDL really 'bad'?

Indeed.

Hormonal havoc and energy balance dysregulation caused by neolithic excess of refined n-6 vegetable oils, high fructose GMO-corn syrup, intestinal permeability, refined carbohydrates, sugar, mercury/arsenic/lead/cadmium, gut dysbiosis, failures of vitamin/mineral absorption by the action of phytates and lectins, and endocrine-disrupting consequences of pesticides and other environmental persistent-organic toxins are more likely factors.

And they have nothing to do with LDL. Half of heart attacks occur in individuals where the LDL is already less than 70 mg/dl.

The old cholesterol guidelines NCEP/ATP-III  that were first put out over a decade ago are now being revamped.  Nature has a new article on the future NCEP/ATP-IV.


'Since 2002, when ATP III called on doctors to push LDL levels below set targets, the concept of low cholesterol has become synonymous with heart health. Patients brag about their cholesterol scores, physicians joke about adding statins to drinking water, and some hospitals reward doctors when patients hit cholesterol targets.'

~~~~~~~~~~~~~~~~~

LDL Affected by Apo E Alleles




Amount of LDL-C and LDL-P Determined by ApoE

We each individually and uniquely have widely varied lipoprotein patterns (LDL, TG, HDL) determined by our genetics, the microniche our ancestors evolved and survived in, and our apolipoprotein E. Apo E is mainly found in HDL and LDL particles but also free form in the circulation as well. It aids lipoprotein particles in docking up to cell membranes to unload contents into a destination cell or the liver.

Apo E determines the LDL-quantity. Three alleles for apoE exist and we each have 2 copies from a mix from our parents - E2, E3 or E4. ApoE to me is like a special key to unlock troubled doors. Those with E4 alleles have lipoproteins with the least apoE (perhaps true H-G, more cholesterol hung out longer in circulation).  Geographically the incidence of E4 rises toward a northern distribution in Europe, away from the equator.  Those with E2, more apoE (perhaps more agarian adapted).  Energy flux patterns and metabolism are mildly different: E4, more carbohydrate sensitive; E2, less.  

Many 'cardiac' rat models use apoE-deficient mice because these animals inevitably develop horrific plaque and atherosclerotic disease and blocked arteries, on high carb rat chow.

The lower the apo E alleles, the lower the total cholesterol [ref 2]. The researchers (above) demonstrate the LDL and HDL trend in parallel with total cholesterol and the higher the E.  Conversely, triglycerides grow higher, the lower the apo E.

It seems finally that the medical community be viewing the true science and questioning the BS.  If LDL is genetically determined by the apoE type and is a false coronary risk factor, then what is the true cause of coronary events, MIs, angina and plaque destabilization? 

Naturally if one is apoE 4/4 (rare), then one is likely to have the highest LDL amongst friends and aquaintances. Is it harmful? Depends. ApoE 4/4 are more likely to be HIGHLY insulin resistant, inflamed and carbohydrate sensitive. In the modern industrial environment where whole food, ancestrally-inclined meals are endangered species... perhaps.  

Are apoE 4/4 the true survivors of Earth? They are less likely to suffer from infections or starvation which were the major reasons for mortality outside of predation prior to neolithic times. Add to that vascular protection from Lp(a) from vitamin C-deficiency hemolysis and one has a winning combination for longevity given the right circumstances when inflammation is well regulated and gene-protein expression optimal. 

The higher the LDL, the higher the Lp(a), the better survival?



Size of LDL Determined by Diet and Lifestyles: Microecological Niche

Environment dictates the LDL-particle-size. Exercise, high saturated fat, cholesterol-intake, low carb, low fructose, low omega-6/omega-3 ratio and antioxidants/flavonoids are factors that high influence and create more large, buoyant, resistant-to-oxidation LDL-particle-sizes, despite apoE status.



LDL Less Than 70 mg/dL is Dangerous

So why are cardiac 'experts' prescribing a one-size-fits-all LDL goal of less than 70 mg/dl and statins for all individuals with heart disease, diabetes, aneurysms, chronic kidney disease, and other atherosclerotic equivalents?

Does this take into account apoE status and genetically-predetermined LDL amounts?

An LDL less than 70 mg/dl is not magic.  At TYP, very rarely did I observe CAC Agatson coronary artery calcification reversal.  Members were on potent statins or suppressed their LDL to (unnatural) goals of 60 mg/dl. 

Seth Roberts did achieve reversal, by consuming cholesterol (butter). No pharmaceuticals.

I have noticed countless, sad times where statins do nothing to regress or stop the progression plaque. In fact, they are associated with progression in 12 out 14 published coronary calcification studies.

Many studies show that statins are also highly associated with cancer, increased incidence of congestive heart failure (CHF), accidents, violent death, depression/suicide, and all-cause mortality.

Low cholesterol and low LDL, independently, additionally are significantly correlated to cancer, increased incidence of chronic heart failure and all-cause mortality.

Let's probe this... because statins lost their allure years ago for me.




Overview of Transporters

Every vital vitamin, hormone and steroid exists both 'free' and available in the blood circulatory system and bound to degrees to a transporter-protein. Some vitamins, hormones and steroids interact directly with receptors on cell membranes and other cases the transporter-protein interacts with receptors on cell membranes to translocate the vitamin, hormone or steroid into the cell. From the gut to the liver, food gets processed into free fatty acids, triglycerides (3 fatty acids attached to one sugar backbone) and bundled into particles with antioxidants for circulation and storage in peripheral tissues like the muscles, adipose, gonads, and adrenals.



Cholesterol

Every cell membrane is composed of cholesterol -- this is the asphalt and infracture of our communication highways. Another way to appreciate these conductors of electronic charge is to recognize that cholesterol in our cellular membranes is analogous to the DSL or Comcast cables of our high-speed computers, our brain and nervous systems.

How do 'dropped signals' feel? Perhaps your cholesterol is impaired?

Roles of cholesterol:
a) formation of cellular walls
b) formation of aldosterone (important for blood pressure regulation)
c) formation of the sex hormones
d) formation of Vitamin D
e) formation of bile to eliminate and recycle wasted and precious fat-soluble molecules
f)  formation of corticosteroids which are involved with glucose regulation and suppressing inflammation

g) formation of steroidal derivatives including the vital and potent antioxidant Ubiquinol/ CoenzymeQ10
h) antioxidant with scavenger functions for harmful microbial endotoxins


Without cholesterol, humans cannot survive, brain and organ function deteriorate, and eventually cancer and other inflammatory conditions are triggered. Without sufficient cholesterol, cortisol, testosterone, progesterone, estrogens and other potent steroidal hormones cannot be made.



Statins Lower Testosterone

As one would expect, statin pharmaceuticals which block the rate-limiting enzyme for cholesterol production in the liver and all extrahepatic sites (e.g. BRAIN, ADRENALS, TESTICLES, etc), HMG-CoA reductase, are highly associated in reduction of total testosterone and subsequent low testosterone signs and symptoms [ref 3-9].

Low testosterone is also considered a risk factor for heart disease due to the inflammatory state that occurs including obesity, metabolic syndrome, hyperinsulinemia, poor immunity and diabetes[ref 7]. I question the prudence in the strategy behind initiating a statin and potentially lowering testosterone further, thereby inducing yet another cardiac risk factor.  Would you like to be a eunuch?

Diabetic eunuch?  Chuckle with Peter at Hyperlipid: 
Sta'ins, CoQ, diabetes and Dr Andreas Eenfeldt's link



Ancient Transporters

Our lymphatics and blood vessels form the highways that transport nutrition, oxygen and necessary constituents for organ maintenance and rebuilding. They also remove wastes, CO2 and recycled cellular parts and spent steroid hormones for elimination via the gut or 'recycling' via enterohepatic recirculation.

How are antioxidants, pro-vitamins, vitamins, pro-hormones and hormones from our food and endocrine glands/tissues carried to the peripheral sites? Ancient tranports have evolved (if you believe in evolution) in all living systems for the role of carrying these items to the appropriate target tissues.

Vitamin A (retinol): free and bound to RBP (retinol-binding protein)
Vitamin D (cholecalciferol): free and bound to VDBP (vitamin D binding protein, aka Gc globulin)
Estrogen (E1 E2 E3): free and bound to SHBG (sex-hormone binding globulin) and EBP (estrogen-binding protein)
Testosterone, DHT: free and bound to SHBG and ABP (androgen-binding protein)
Progesterone: free and bound to SHBG and PBP (progesterone-binding protein)
DHEA: free and bound in HDL particles
Cortisol: free and bound to CBP (cortisol binding protein)

Ubiquinol/CoQ10:  bound in HDL and LDL
Menaquinones (MK4 to 9; vitamin K2):  bound in HDL and LDL
Retinoids (vitamin A):  bound in HDL and LDL
Carotenoids (vitamin A): bound in HDL and LDL
Tocopherols, tocotrienols (vitamin E): bound in HDL and LDL
Minerals - iodine zinc selenium copper: Free form and bound in HDL and LDL
Cholesterol: Free form and bound as Esters in HDL and LDL


See prior animal pharm: LDL, HDL Transporters



Purpose of LDL and HDL Transporters: Evo Perspective

Lipid transport and delivery systems existed in the earliest animals including insects. Our lipoprotein systems are not that dissimilar [ref 1]. Fat-soluble nutrients like cholesterol, carotenoids, vitamin E and coenzyme Q10 would form a two-layered oil-vinegar like concoction in our blood circulatory system if it were not for specialized transporters for fat-like substances.

HDLs are much more compact and smaller in size than LDL. They fit between the gap and communication junctions in the endothelium (lining of blood vessels). Whereas, LDL particles are larger and barely fit between normal gap junctions of endothelium. If the LDL particles however are 'small' their purpose is different. They are more oxidizable and denser. This tighter conformation allows movement into damaged endothelium and traumatized and inflammed tissues to provide ammunitions for macrophages to do their work and relinquish the waste and end products for disposal. I don't read French (see below if you do).

Once HDL and LDL are done, they can re-enter the blood stream, return to the liver for future processing.







Ubiquinol Protects Against Failure of the Heart and All Organs

Ubiquinol is lowered by statins since ubiquinol and its derivatives are cholesterol structures [ref 19]. Unfortunately ubiquinol is necessary in all cells and mitochondria where it serves a role as mandatory antioxidant and a recycling nazi [16-18]. Low ubiquinol in the blood is associated with faster progression of heart failure [ref 17].

Statins lower the LDL contents of ubiquinol and all fat-soluble nutrients, vitamin E and carotenoids. Does this have consequences?

Prior animal pharm: Role of Ubiquinol



Higher the Cholesterol, Higher the CHF Survivorship


Our understanding of survival and the evolution of insulin resistance provides the foundation to understand the causes of all diseases of modern civilizations including CHF. The studies bear this out in which the higher glucose and higher insulin resistance, the higher the association to mortality in CHF [ref 12-16]. Interestingly several studies demonstrate the lower the cholesterol, the higher the CHF mortality. Some clinicians raised the potential risks of statins in light of these adverse outcomes in individuals with CHF [ref 31].

In patients with progressive CHF, their LDL are all small packages which can barely hold vital antioxidants like ubiquinol. Add a statin which deplete the crucial functioning ubiquinol for pumping heart muscles, spelling catastrophe.




Low Cholesterol Associated With Increased Cancer Incidence: 17-Year Basel Study 

The prospective 17-year Basel study showed a 2-7 fold increase in cancer mortality in males at various cancer sites with low serum cholesterol. This study confirms what some of the other cancer epidemiology studies have already shown. Researchers tested blood from 2974 participants stored from 1971-1973. Co-founders such as vitamin blood levels were adjusted for in the analysis.

Quality will always trump quantity of LDL.


Prior animal pharm: Cardio Controversies -- Tale of 2 LDLs




Carcinogenicity of Statins: The Lower the Final LDL, the Higher Cancer Rate


Finally the statin and lipid-lowering drug trials themselves have demonstrated that the lower the cholesterol, the higher mortality from cancer in a meta-analysis in JACC, 2007 by Alsheikh-Ali et al [ref 27]. Plotting final LDL with cancer, the graph depicts a firm association between the lower the LDL and increased cancer incidences.





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J Am Coll Cardiol. 2003 Dec 3;42(11):1933-40.

14. Impaired insulin sensitivity as an independent risk factor for mortality in patients with stable chronic heart failure.
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20 comments:

Calvin said...


Chip Spitter said...

Good post, thanks for your continued work in this area. Being an E4/E4, I always like to read more about it, even if there's chance it is just confirmation bias.

Have a good one.

Anonymous said...

I think you mis-cited the last paragraph? Ref[27] is a meta-analysis of rodent studies, but the figure you posted is from: "Effect of the Magnitude of Lipid Lowering on Risk of Elevated Liver Enzymes, Rhabdomyolysis, and Cancer", which you didn't cite.

George Henderson said...

Great post and good to hear from you again. Everyone needs to know this stuff.
Seems to me some interventions - fish for example - might lower LDL (maybe, I'm not certain it does) - in ways that don't compromise health (activation of PPAR-alpha meaning slightly more fat burned in liver instead of exported). Others might elevate LDL (eating a big chocolate cheesecake everynight) but compromise health due to glucose-insulin loads and empty calories.
So it's not the rise or fall in LDL per se, but whatever caused it. And as very different things and different processes can cause similar-looking changes in LDL and HDL we should ask are those THINGS desirable in our lives - and bugger the cholesterol numbers they result in. A cholesterol number should never cause you to consume a harmful thing or avoid a nutritious one. IMO.

Dr. B G said...

Anon --
Thnx! Fixed. Both statins and controls actually have increased incidence of cancer at the lower LDLs. In rodents any dose of statin is carcinogenic. Humans are different but I'm not sure how.


George,
I appreciate the posts on your blog as well. FASCINATING STUFF ;)
Yes I try not rely on labs but sometimes one has to (love/hate). Being in China, obtaining labwork is challenging to say the least. For instance many on statins have no idea they are doing harm to each and every mitochondria (particularly liver ones, no?). Muscle punch biopsy studies have demonstrated damage to muscles due to statins despite totally 'normal' CPK.

Phillips PS, Haas RH, Bannykh S, Hathaway S, Gray NL, Kimura BJ, et al. Statin-associated myopathy with normal creatine kinase levels. Ann Intern Med 2002;137:581-5.

England JD, Walsh JC, Stewart P, Boyd I, Rohan A, Halmagyi GM. Mitochondrial myopathy developing on treatment with the HMG CoA reductase inhibitors - simvastatin and pravastatin. Aust N Z J Med 1995;25:374-5.


Labs are just a surrogate for what a person is trying to discern objectively.
http://drbganimalpharm.blogspot.jp/search/label/SHOW%20ME

UR RIGHT ON. So many limitations! I enjoyed your example of trends with fish v. cheesecake. Depending on the person (E2 v. E4) LDL may go up or down!

Dr. B G said...

Objective ways to assess function and health of mitochondria (and statin damage) is to measure mitochondrial CoQ10, TCA and Kreb cycle intermediaries and organic acids.

http://www.metametrix.com/learning-center/articles/2006/why-test-for-coenzyme-q10

Chris Woods said...

I'm a 4/4 and want to thank you for your continued review of the research. Whereas most most opinions conclude that 4/4 is a frail mutation, I agree with you that it conveys benefits given the right environment:

- Inconsistent access to high quality nutrients, calories
- Less abundant sunlight exposure on the skin
- Little exposure to heavy metals, vegetable oils & sugars
- Lots of movement
- Intermittent high stresses rather than prolonged low-level stress (certainly applicable to all mutations, but moreso for 4/4s)

I suspect trying to replicate that environment will lead to best chances of disease-free longevity.

Dr. B G said...

Mr. Chris Woods,

U GIT IT!

I'd love to hear what else you've learned ;)

Yes to me the evidence points to minimization of oxidative stress and inflammation as particular keys to E4/E4 longevity. On his latest podcast, Robb Wolf pointed out with great clarity and insight that E4 carriers have had an evolutionary trade-off: higher inflammatory immune defenses against parasites and worms.

I have noticed that certain phenotypes ('warrior') have super effective immune systems, and perhaps E4 is one.

I've met a half Yaki Native American (Californian) who told me as a kid he would watch his wounds heal right in front of him.

Super 'healers' also have super coronary and brain plaque when oxidizing agents are introduced into their biological systems -- refined carbs, HFCS, sugar, mercury, cadmium, aluminum, arsenic, persistent organic pollutants, pthalates, pesticides, fungicides, etc.

Many in the integrative medicine field like me believe that 99% of everyone has heavy toxic metals. The only 1% that don't are the ones who have chelated. People eat a fish; unfortunately they all have mercury now even the wild salmon.

Gdx/Metametrix have great non-invasive testing (easy-pay makes insurance easier now).

Consider these resources:

http://www.slideshare.net/metametrix/porphyrins

http://www.metametrix.com/files/test-menu/interpretive-guides/porphyrins-ig.pdf

http://www.metametrix.com/files/learning-center/leifm/Urinary-Porphyrins.pdf

Alex said...

I'm also E4/E4, and carbohydrate sensitivity has been an issue for me my entire life. Unfortunately, I let new-age dogmas about the idealness of whole grains and beans override my body's own wisdom, and it was not until 30 pounds of subQ flab was drooping from my body that I moved in the direction of paleo and lost all that weight. My appetite, blood sugar, and energy levels get messed up by starches more than anything else, so I eat low-ish carb, with carbs from fruits and veggies making up about 25-30% of calories. Fat is about 50-60% of calories. Caloric intake is such that I maintain my weight at 170# at 6'1". I've seen all sorts of conflicting recommendations for E4s, and with Alzheimer's sometimes described as diabetes of the brain, I figure the best dietary strategy is one that maintains endocrine serenity.

Dr. B G said...

Alex,

U LUCKY ANCESTRAL BRAINIAC

Thank you for your thoughts. I strive toward 'endocrine serenity' too... LUV THAT

The major inflammatory markers actually are not elevated in E4 carriers, interestingly. Some think the inflammation is independent of E4. E4 are shown to have lower hsCRP, homocysteine, TNF, and IL6.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2908458/

http://circgenetics.ahajournals.org/content/5/1/e1.full



I concur -- I think inflammation for E4 stems from exogenous sources: virus, bacteria, microbes/fungus, worms, parasites, blunt force infections, toxins, heavy metals, etc. E4 carriers overproduce LDL-P, and particularly oxLDL (small dense LDL) under circumstances.

Lp(a) in the face of vitamin C (subclinical to full-on scurvy) or other oxidative stressors is inflammatory and the selective pressure was to patch up holes created by vitamin C-collagen dependent ulcers in the endothelium and organs.

Like low vitamin C, mineral and other and micronutrient deficiencies would cause similar patterns without the 'need' for hyperactive stress responses like TNF, IL6 or homocysteine, no?

Environmental toxin load challenges E4 carriers. So the E4 carriers with variants for detox and DNA methylation may be the only ones who have problems with modern toxins and diets, since infections are better controlled with sanitary water, etc. (on the flip side, gut dysbiosis may be more challenging and oxidative)

One study showing more ancestral variants of DNA methylation and LDL-R polymorphisms in E4 carriers:

http://www.ncbi.nlm.nih.gov/pubmed/21461956


Reduced cognition only when apoE4 + MTHFR, not E4 alone or MTHFR alone:

http://www.spanishexernet.com/pdf/Adolescentes%20nuevo/RuizJR_2010JPediatrics_cognitive%20performance.pdf


So, heightened oxidative infectious potential + disabled detox + trigger = bad

Dr. B G said...

BTW, yes, also, agreed. Many people don't get E4. MDA recently posted on E4 and I think it was wrong based on the science. I wish the worker bees did their homework!


William Davis' site TrackYourPlaque has a lot E4 carriers. NONE achieve regression (99.5% of the site) unless the xenobiotics were limited (drugs, statins, refined carbs etc) and saturated fat/cholesterol GREATLY INCREASED.

Nutritional studies on apoE show that E4 NEED dietary chol and saturated fats MORE than E2 and E3 to maintain healthy (buoyant) LDL, HDL, Lp(a), VLDL. Controlling insulin resistance (low carb, low toxins, mercury/arsenic chelation, adequate exercise, etc) is key, not 'low fat diets'...

Anonymous said...

So glad you are posting on this subject, Grace. I lived through years of statin therapy and once I gave up statins my testosterone levels normalized. My HDL2B also doubled from high intake of fats including saturated, MCT and monosaturated. I finally came to realize the cholesterol hypothesis was a mere myth. Aerobic1

Dr. B G said...

Hello Aero--

Thank you for your comment. Congratulations for your eyes opening. It is never too late I believe. Compounding the T-lowering effects was probably the high-blood-glucose-inducing, low-fat and egg-avoiding diet!

I hope Americansoon reclaims its TESTOSTERONE (and HDL2b) as you have done so wonderfully and easily.

Many though will have a hard time and continue to believe all the fairy tales spun by conventional medicine paradigms because they are not aware or interested in therapeutic options.

It is good to see vocal mainstream docs like Dr. Stephen Sinatra and DR. Oz, who do not fear vindication by statin-demented NCEP/ATPIII drug pushers (I know - I used to want to put it in the water).

Love the title of Sinatra's new book 'The Great Cholesterol Myth: Why Lowering Your Cholesterol Won’t Prevent Heart Disease-and the Statin-Free Plan That Will.'

Sounds like you know the protocol and could write the book!

Oz has two video clips that actually I am quite impressed. He sounds like an integrative practitioner now.

http://www.foodrenegade.com/great-cholesterol-myth/

(from food renegrade)
--How total cholesterol levels don’t matter!
--How statins are dangerous — particularly for women.
How what really matters is the size of your cholesterol, not the kind.
--How high blood sugar levels can lead to arterial inflammation.


And the interview with Johnny Bowden together with Sinatra -- Is everything you know about cholesterol wrong? Part I

http://www.doctoroz.com/episode/doctors-who-say-everything-you-know-about-cholesterol-wrong

Lou said...

Thanks for this excellent insightful article.

What is the real problem with taking toxic (Statins are EXTREMELY toxic) "drugs" whose NUMEROUS effects are unknown, to try and achieve a incompletely measured body state, using a model which may or may not be correct, which may or may not improve our health?

Well I believe I just told you.

Dr. B G said...

Thx Lou! I'm grateful you are bright

lightcan said...

Hi G.,

How are things?
What do you think about LDL-Nb reaction to changes in the environment? My LDL skyrocketed in reaction to 2 year long low-carb diet. (it's like the joke 'The operation was successful but the patient died'. I lost the weight but my health got worse in other ways) The endocrinologists didn't care about my low T3 and free T3, saying it's normal on weight loss diets and didn't connect the dots. Low dose T3 therapy caused LDL to get back to baseline (still high but went down more than 100 %!) but suppressed my TSH and turned off my thyroid. To which the 'consultant' says it must be the reduced sat fat that sent down my LDL!?
He wants a repeat, obviously, which I avoided for the last 2 years. I don't intend to eat a low-fat diet.
I'm trying to lose fat again, unfortunately (it was very hard getting out of a dependency state but I did it), and I'm going to be more careful with the carbs this time.
I haven't had a respiratory infection in ages, however I had aggressive gum disease that was identified in 2000, only stopped in 2007 and that destroyed a lot of the bone supporting the teeth. I have to go to the hygienist every 3 months. What does that say about my body?
I thought I had a high Lp(a) result somewhere but I can't find it. I always thought that it is the long term exposure to mercury amalgams and the fluoride that I'm exposed to since 1998 that changed things. I don't know. Skin tags point to high insulin, which could be due to years of excess calories.
I wish I understood the causes so I knew my body better.

lightcan said...

I meant to say LDL went down 50%.
I wonder is it a simple case of cells not accepting the LDL or of ramped up LDL production (VLDL) for immune function or both.

Dr. B G said...

lightcan,

I wouldn't worry too much about the LDL going up or down (or the Lp(a)). Thyroid regulates the LDL receptors so when hormones are optimal, then the LDL particles will be anti-inflammatory, large, and buoyant. The TG/HDL ratio is often more revealing than an absolute calc LDL.

For those with FHC and/or apoE4, LDL is naturally higher than average and not problematic unless under inflamed circumstances (toxins, low thyroid, low progesterone, estrogen dominance, infections, pathogenic GI overgrowth, mental stress, etc).

Have you considered the adrenal and gut health and toxic accumulation of mercury and other exposures (arsenic, lead, aluminum, solvents, PCBs, pesticides, etc)?

Do you walk or exercise?
Do you engage in meditation or yoga?
Have you read Schwarzbein on how to recover from LC/ketosis related metabolic damage?

Unfortunately I found that I had to gain 5-10 lbs before my metabolism was fixed after doing ketosis/endurance sports for WAY WAY WAY too long. The adrenals are the key -- keep them happy. Thyroid shouldn't be treated in isolation from adrenals. For me, my adrenals couldn't perk back up until all the mercury and titanium were extracted.

Good luck!

I'm sorry about the delay in responding. Feel free to email for quicker responses!
G

Dr. B G said...

Also lightcan, there are a lot 'paleo' esque habits which I think are all terribly, very bad for adrenal health. All the below can promote adrenal exhaustion, low T3 and high rT3. Girls are prone to adrenal stuff because we gender wise don't tolerate IF. This is in several clinical trials as well. We bear children -- we produce glucose and ketones both heavily during gestation. We are not as glycolytic as males, which puts strain on the adrenals because glucose production (gluconeogenesis) requires adrenaline and cortisol synthesis from the adrenal glands.

--coffee
--coffee + chocolate
--bulletproof coffee
--fasting
--bulletproof coffee + fasting
--intermittent fasting
--skipping meals
--LC (low carb)
--ketosis (no carbs < 20g/day)
--Crossfit
--Metcons/tabata etc things that spike the HR for susceptible people
--LC/ketosis + Crossfit
--LC/ketosis/IF + Crossfit/Metcon/Tabata
--etc


Get the idea? Don't find out the hard way... All the above are forbidden on any adrenal recovery protocol.

lightcan said...

Thank you G.,

I do not drink coffee. I will not do IF, skip meals or LC. I don't exercise or meditate. I know I should.
I got my bloods back. The thyroid hormones look OK. TSH 1.28.
TC high again. TC 9.41 (364), LDL 5.93 (229), but HDL 3.27 (126) and trigs 0.46 (41). (diet less than optimal and 14 kg extra)
Others: poor sleep (high cortisol at night?), stress (feeling of overwhelm), no oxyt., mercury fillings, probably low progesterone or estr dominance (luteal phase problems), gut health not great (constipation and acne/skin inflam.)
If it weren't for you and dr Sara I wouldn't even know about adrenal problems.