Does this include the beta sitosterol that is in most prostate supplements?

How can I get tested for sitosterolemia?

I know for a fact that Costco sells 5000+ bottles of CholestOff every WEEK! The stuff is a blend of sterols.

Yeah costco also has "sterol" oatmeal bars.

I try to stick to the freezer and wine section.

I like how you state plainly it's "rare," and now your followers are going to start to believe themselves to have this ailment. I like your blog, but as of late, you're war on heart disease is imitating the ad baculum aspects of America's war on terror.

Excellent article. I've had the same exact thoughts and that's why I don't take supplementary plant sterols.

It's pretty comical. When people supplement with sterols, all they are doing is swapping some of their cholesterol in LDL particles with sterols. The sterols essentially take the place of the cholesterol in the blood. But both have the proclivity to cause atherosclerosis.

So, the cholesterol lowering effect is just an illusion.

I'm not so sure Apo E4 would even be considered 'rare' amongst those who have heart disease problems... or who are considered high risk.

E4/E4 is quite rare, but E3/E4 isn't really. I think it's around 25% of the population, if I recall correctly. And I'd expect amongst those with heart issues, it'd be higher than that.

So what do you eat if you are disp. to Apo E4. If I eat sat. fat my LDP
rocket up. If I eat more veg. and fruit and lean mead it rocket dovn.
Am I on the track??

Hi, Kathy--

Yes, it does.


Lucy--

In general, testing for sitosterolemia is not something I would recommend except in specific situations, in which case the various sterols in the blood can be measured.

That was not the point of the discussion, but the far more common Apo E4 that affects 25% of the population, who thereby potentially hyperabsorb sterols.

For those wanting to follow up on the role of Apo E4 here is an interesting article.
APOE-4: The Clue to Why Low Fat Diet and Statins may Cause Alzheimer's by Stephanie Seneff

I tracked it down after reading
Nutrition and Alzheimer's disease: The detrimental role of a high carbohydrate diet
I never thought I would read in a peer reviewed paper the words The strong influence of Ancel Keys, beginning in the 1960s, has led to dietary avoidance of fats and cholesterol along with over-zealous prescription of cholesterol-reducing medications over the same decades in which there has been a parallel rise in AD prevalence."

Ted,
I can do you one better. This prospective cohort study (n=1137) found "Higher levels of HDL-C (>55 mg/dL) were associated with a decreased risk of both probable and possible AD and probable AD compared with lower HDL-C levels (hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03 and hazard ratio, 0.4; 95% confidence interval, 0.2-0.9; P = .03). In addition, higher levels of total and non–HDL-C were associated with a decreased risk of AD in analyses adjusting for age, sex, education, ethnic group, and APOE e4 genotype." Here's the link to the abstract:  http://archneur.ama-assn.org/cgi/content/abstract/67/12/1491.
Makes you wonder the REAL reason behind statin drugs.

I used beta-sitosterol for over a year.  I used it because I didn't want to take a 5-alpha reductase inhibitor such as Proscar.  But I developed the same side effects that Procar is known to cause:  Poor libido, gynecomastia and generalized muscle weakness.  I don't track cholesterol so I don't know what the beta-sit might have done to it.  Six months off the beta-sit and I'm just now starting to feel like a normal man again:  morning wood, etc.

That was my reason for asking... because I'm a 3/4

Both links are to the second study.
The correct link for the first study is:

Alterations in cholesterol absorption/synthesis markers characterize Framingham offspring study participants with CHD

Fructose Alters Brain Metabolism
One of the competing theories to explain the obesity epidemic is a rise in fructose consumption causing alterations in hormone levels that increase appetite. UCSF med school prof Robert Lustig has a pretty good rant-lecture on the evils of fructose. Well, here's another study on part of the mechanism in the brain of how fructose might be causing increased obesity.

PORTLAND, Ore. – The dietary concerns of too much fructose is well documented. High-fructose corn syrup has become the sweetener most commonly added to processed foods. Many dietary experts believe this increase directly correlates to the nation's growing obesity epidemic. Now, new research at Oregon Health & Science University demonstrates that the brain – which serves as a master control for body weight – reacts differently to fructose compared with another common sweetener, glucose. The research is published in the online edition of the journal Diabetes, Obesity and Metabolism and will appear in the March print edition.

In humans the cortical brain control areas of the brain were inhibited by the influx of fructose.

Functional MRI allows researchers to watch brain activity in real time. To conduct the research, nine normal-weight human study subjects were imaged as they received an infusion of fructose, glucose or a saline solution. When the resulting brain scans from these three groups were compared, the scientists observed distinct differences.

Brain activity in the hypothalamus, one brain area involved in regulating food intake, was not affected by either fructose or glucose. However, activity in the cortical brain control areas showed the opposite response during infusions of the sugars. Activity in these areas was inhibited when fructose was given but activated during glucose infusion.

This is an important finding because these control brain areas included sites that are thought to be important in determining how we respond to food taste, smells, and pictures, which the American public is bombarded with daily.

The result increases the plausibility of fructose as a causal agent.

"This study provides evidence in humans that fructose and glucose elicits opposite responses in the brain. It supports the animal research that shows similar findings and links fructose with obesity," added Purnell.

If you want to reduce your weight also consider other theories for the cause of obesity including grains as a possible major cause.

By Randall Parker 2011 February 09 05:42 PM  Brain Appetite

Hi, Peter--

Thanks for catching that.

Now fixed.

Foods with naturaly occuring levels of Beta-sisterol: fruits like avocado, nuts like pecan & cashew, seeds like flax & pumpkin,
legumes like soya & peanut, grains like wheat germ & rice bran, oils like corn & soy, plus herbs like Saw Palmetto & Pygeum. Once again it is good to recall that if something is good for you that doesn't automaticly mean more is better for you.

@Anon about naturally occurring sitosterol levels -

As an APO E4 person, should I be concerned about my intake of avocado, flax seed, and tofu?

couldn't leaky gut syndrome cause increased sterols in the bloodstream?

So... how much sterols?
For example almonds and other nuts are high in sterols. Lot of vegetables are high in sterols. In this blog nuts have been recommended often as well as a plant based diet. So does this change that?
What should apoe4 people eat? They can't eat fat, now they can't eat vegetables? Is starving to death the only way to avoid heart disease?

Also tofu and soy has been promoted which have esterols...

Another benefit to total avoidance of plant oils!

Miniscule n-6 means miniscule fat soluble sitosterols.

Are you ready to advocate an animal-fat based diet for ApoE4 and the 45 total reported cases of sitosterolemia?

If you worry about LDL, ApoE4 needs to be "low fat", but if you worry about early death and AD, I think high animal fat is the way to go for these folks.

Isn't the problem for APOE4 the way the molecule degrades? Quite recently fish oil Omega 3 has been cited for allaying APOE4's side effects. The Omega 3 balances out the metabolite (an APOE4 protein fragment) that otherwise messes with the lipid structure of the mitochondria(s) membrane(s); it (fish oil) prevents dysfunction.

http://m.npr.org/news/front/139889533

I heard a report on this study on NPR yesterday.  It's important to note who sponsored the study in the first place.

Then again it maybe this patient was using too low a dose?
And what else was the patient ingesting? And there is the issue of which class lipid abnormality this patient had.

In my comments below I've included some abstracts of some human based studies that suggest inositol hexanicotinate isn't useless for altering serum lipid levels.


If we assume for a moment the validity of your anecdote,
I won't call inositol hexanicotinate worthless rather I would suggest it might have has narrower scope of uses not including the altering
blood lipids.  Not everyone (me) takes large doses niacin for it lipid altering properties. Consider Kaufman's work with niacinamide in patients
with degenerative arthritis. He used doses of 1.5 to 4 grams and
claimed increased joint mobility after a couple of months.
In my experience, niacin also works as well as niacinamide
against my pains in and around my joints. Its benefits against the pain come about gradually but
nonetheless are quite effective for me.

The flush can be pretty nasty if one isn't careful about the dose.
I know when I mixed niacinamide and niacin in the past I seemed
to have somewhat more flushing. I took niacin for several years
until it started to be trigger atrial premature beats.
I'll comment further in this posting on a way around these adverse effects of niacin.


Inositol hexanicotinate maybe superior provided one chooses
the right patients? Please see the second abstract below.
----------------------------------------------------


1: Eur. J. Clin. Pharmacol. 1979 Aug;16(1):11-5.


Nocturnal inhibition of lipolysis in man by nicotinic acid and derivatives.


Kruse W, Kruse W, Raetzer H, Heuck CC,
Oster P, Schellenberg B, Schlierf G.


The effect of nicotinic acid and several derivatives
on the nocturnal level of free fatty acids was studied
in 12 healthy young women and men. Free fatty acids
are an important precursor of plasma triglycerides
and their concentration is highest at night.
The drugs used were nictinic acid, beta-pyridyl-carbinol,
mesoinositol hexanicotinate and xantinol nicotinate.
The highest plasma nicotinic acid level was observed
with beta-pyridyl-carbinol, but significant reduction in
free fatty acids during the entire night was only
achieved with inositolhexanicotinate and
xantinol nicotinate. There was no correlation between
the plasm levels of free fatty acids and nicotinic
acid at any sampling time. If prolonged reduction
in free fatty acid concentration is desired in the therapy of
hyperlipidemias, the inositol and xantinol esters of
nicotinic acid appear to be superior to the other preparations.


PMID: 499296 [PubMed - indexed for MEDLINE]
========================================


Inositol hexanicotinate seems to work to lower some
blood lipids in this next human study and granted
another drug is also involved.
-------------------------------------------------------------
1: Arzneimittelforschung. 1979;29(10):1621-4.


[Treatment of various types of hyperlipoproteinaemia with
a combination of Mg-chlorophenoxy-isobutyrate and
mesoinositol-hexanicotinate (author's transl)]


[Article in German]


Bolzano K, Krempler F, Haslauer F.


50 patients with different types of hyperlipoproteinaemia
were treated with a combination of Mg-chlorophenoxyisobutyrate
(700 mg) and mesoinositol-hexanicotinate (500 mg) (Atroplex)
twice daily. 7 patients had type IIa, 39 patients type IIb
or IV and 4 patients type V. After a period of one
month without any treatment the patients were treated
during two months. While the effects of this combination
on cholesterol of type IIa patients was poor, the
drug had an excellent lipid-lowering effect in the patients
with type IIb, IV and V. After 14 days' treatment the
plasma cholesterol and triglyceride levels in
patients of type IIb or IV were significantly lowered.
This effect became even more pronounced after
one-month treatment. There was no significant difference
between the effect of one-month treatment and
that of two-month treatment. About two-thirds of the
patients of type IIb or IV were responders. No serious side
effects could be observed during our study.


Publication Types:
    English Abstract


PMID: 583231 [PubMed - indexed for MEDLINE]
--------------------------------------------------
So could it have been that this patient had one of the classes
of hyperlipidemic disorders such as type 1, type
2-a or type 3 for which inositol hexanicotinate
maybe ineffective?


=====================================================
It may have other uses see next paper.
-------------------------------------


1: Clin. Rheumatol. 1988 Mar;7(1):46-9.


A double blind randomised placebo controlled trial
of hexopal in primary Raynaud's disease.


Sunderland GT, Belch JJ, Sturrock RD,
Forbes CD, McKay AJ.


University Department of Surgery,
Glasgow Royal Infirmary, Scotland.


The peripheral vasospastic symptoms associated
with Raynaud's disease continue to
be an unsolved clinical problem. Hexopal
(Hexanicotinate inositol) has shown
promise in uncontrolled studies and its use in
patients with Raynaud's disease may reduce such
vasospasm. This study examines the effects of
4 g/day of Hexopal or placebo, during cold weather,
in 23 patients with primary Raynaud's disease.
The Hexopal group felt subjectively better and
had demonstrably shorter and fewer attacks of
vasospasm during the trial period.
Serum biochemistry and rheology was
not significantly different between the
two groups. Although the mechanism of
action remains unclear Hexopal is safe
and is effective in reducing the vasospasm
of primary Raynaud's disease during the winter months.


Publication Types:
    Clinical Trial
    Randomized Controlled Trial
    Research Support, Non-U.S. Gov't


PMID: 3044673 [PubMed - indexed for MEDLINE]
====================================================
: J. Int. Med. Res. 1979;7(6):473-83.


An experimentally controlled evaluation of the effect
of inositol nicotinate upon the digital blood flow
in patients with Raynaud's phenomenon.


Holti G.


The vaso-active effects of inositol nicotinate (Hexopal)
were investigated in thirty patients with primary and
secondary Raynaud's phenomenon using several
non-invasive experimental techniques under
controlled conditions. The earlier formed impression
that this drug requires a prolonged 'build-up' period was
confirmed. Recording the time required to induce
Raynaud's phenomenon as well as assessments of total
and nutrient digital blood flow showed significant
beneficial therapeutic effects upon the skin's
microcirculation by inositol nicotinate. This study
suggests that the therapeutic effect of this drug is not
merely due to vasodilation but that other mechanisms
such as enhanced fibrinolysis and lowering of
serum lipids may play a significant part in its
overall effect. Smokers responded slower than non-smokers,
but even elderly patients with longstanding vasospastic
disease showed measurably improved digital circulation.
Unlike some other drugs in this field inositol nicotinate was found
to be effective orally and to be devoid of unwanted side-effects.
However, in the majority of patients it failed to
abolish their increased vascular spasm although
it diminished it significantly in most. It appears
to be a safe and well tolerated drug, which,
together with other symptomatic measures, merits
to be used in the management of vasospastic
disease of the extremities even in the
presence of partial obliteration of the microcirculation.


Publication Types:
    Clinical Trial
    Randomized Controlled Trial


PMID: 391622 [PubMed - indexed for MEDLINE]
=======================================


Perhaps what is needed is a larger dose in comparison
to other forms of niacin?

---------------------------------------------
Now to expand the topic to plain old TR niacin and betaine.
---------------------------------------------

Timed release niacin as I recall is twice a effective
as simple niacin in lowering lipids and twice as toxic.
So it seems come out about even if one takes a half
the dose of TR niacin.

Of course, what I'd love to test is niacin in its various forms
along with trimethylglycine (TMG) aka betaine. And I won't  
just consider lipid level effects but also the effects on
osteoarthritis and other joint pains.

Why do I mention betaine? I know from personal experience
high doses of betaine along with niacin pretty well blocks
the flushing effect as well as completely
blocking the atrial premature beats (AVB) that I would get
when taking either high dose niacin or niacinamide.
I had taken niacin at a rather high doses for about 5 or 6 years
back a couple of decades ago and then I started
to get the AVBs when I tried to
resume the use of doses above 100 milligrams.
Now of course provided I take the betaine I don't have
this problem. However, I do get AVBs if I don't use the
betaine and only take the niacin.
Granted some suggest niacin lowers the lipid levels
by "stressing" the liver so if betaine blocks
this effect it maybe contraindicated for the purpose
of changing lipid levels.
Here are Pubmed ID numbers, for some papers that
reflect similar thinking using betaine to reduce
the toxicity of high dose B-3.
PMID: 10985907
PMID: 17156888

--------------------------------------------

I'd be interested in your comments on the points of
theory and science. I am not looking for personal
advice. A number of people including myself
are discussing the niacin topic on the
Usenet forum....sci.life-extension (which
is also available by way of the Google Group
Archive for free provided you have a throw away email address).
Someone else referred to your blog comments and yet
another person proposed contacting you for a comment.
I was elected to contact you.
The group/forum members were interested as to whether there is
more to your anecdote concerning the possible ineffectiveness
of inositol hexanicotinate as a lipid lower agent.

Thank You.

Thanks for your insightful comments.

My experience is based on the experiences of about 10 patients on the no-flush preparation in doses of 1000-4000 mg per day.

If the rationale for the no-flush preparation is that it provides niacin in such a way as to avoid the flush, we should see rises in HDL, reductions in triglycerides, small LDL, and lipoprotein(a), regardless of the type of hyperlipidemia present (IIa, IIb, III, etc.).

After using no-flush for up to one year, I have seen absolutely no effect, accepting my relatively small experience.

Please also understand that my focus is prevention and reversal of coronary heart disease, something that the Track Your Plaque approach does exceptionally well, so I try not to stray off too far from our focus. But why would no-flush have any beneficial effects on arthritis, etc.,as an alternative method of delivering niacin when niacin itself does not possess these effects? I'm not sure I follow the rationale. To be included in a program of coronary atherosclerotic regression, we would have to see substantial effects, as we do with plain old niacin.

Nonetheless, I encourage your continuing interesting thoughts.

Just Friday, a 41-year old woman came to my office for consultation because her doctor didn't know what to do with lipoprotein(a). She had seen a cardiologist who told her to take no-flush niacin. Both the cardiologist and the patient were therefore puzzled when lipoprotein(a) showed no drop and, in fact, was slightly higher on the no-flush preparation.

Could vitamin D be the magic bullet that cures heart disease? Not such good news for drug companies but good for everyone else.

Are the >= & <= symbols correct in the data article?  (target fasting lipid values of: LDL cholesterol >= 60 mg/dl, HDL <= 60 mg/dl and triglycerides of >= 60 mg/dl and a serum level of 25-OH-vitamin D3 of <= 50 ng/ml)  Are they reversed from previous discussions or am I mis-reading them?

King--

Thanks for catching that. The symobols are all indeed reversed. The abstract, curiously, was not submitted that way.

I also noticed that Susie Rockway also did the following study:

Short-term Changes in Lipoprotein Subclasses and C-reactive Protein Levels with the Low Carbohydrate and Low-Fat Diets
Christy C Tangney, Colene Renee Stoernell and Susie W Rockway

If I understood correctly, a low-carb diet appeared to be beneficial in reducing small LDL.

Dr. Davis I know you answer very few of the comments anymore but I was just wondering if Dr. Agatston ha seen your findings and why is he still saying to this day that there is no such thing as calcium score reversal ?

You're right!

Our full findings in the same group of people is due to be published in a journal this summer. I will forward it to Dr. Agatston.

Dear Dr Davis

I would love to read the full abstract of this. I bought the 'Track your Plaque' book just two months ago and had a heart scan which revealed that I did not have any coronary vascular calcification. I'm pleased I have the 'Track your Plaque' book as I feel that preventative medicine is important, and as much knowledge that we can have as possible is a good thing, but it would seem that this book is now out of date as there's very little in it on vitamin D....in fact it isn't even in the index ! Still, I do not feel I can justify the additional expense of becoming a Track Your Plaque member just to read the full abstract and I can't see any other reason for me joining. Will you be publishing this abstract anywhere else ? Or will you at least write more about the importance of vitamin D on your blog sometime ? I entered how much I took in your survey !

with kind regards,
Anne