Xenocal (Orlistat) fat blocker and statins?

[Linda W]

Has anyone combined a fat blocker like Xenical or the OTC fat blockers with statins? My husband is taking Vytorin and having serious emotional issues (see my posts Vytorin). While looking through his meds I remembered he takes Xenical in his effort to get his weight down to a healthy level. In researching the effects of that drug on cholestrol I see it lowers cholestrol by an average of 8% and improves LDL/HDL ratios. My hausband has lost 40 lbs in the last 10 months and improved his diet and exercise routine plus 10 months on Vytorin. It seems like he has reduced his cholestrol to a point where his brain can't function normally. He is on his 3rd day without Vytorin and we are going to talk to his doctor tomorrow. This morning he was pretty depressed and said he feels like he is losing his mind.

[bunnylady]

I beleive that's the brain fog that comes about with the statins- the doctor will say its not the statins but I'd get off it and try it naturally- cinnamon capsules lowered my cholesterol quite a bit

a breakfast of good oatmeal and cinnamon sprinkled on it is a good bet

[Brian C.]

Unfortunately cinnammon lowers cholesterol by a statin-like interference with the mevalonate pathway. I no longer take it.

Brian.

[adec]

[quote="Brian C."]Unfortunately cinnammon lowers cholesterol by a statin-like interference with the mevalonate pathway. I no longer take it.

Brian.[/quote]

Good morning Brian. Hope everything is well on your side of the pond. Yeah, I honestly don't know from where this overall conclusion comes. Do you have a link? Cinnamon oil *at best* is a benignly mild CoA reductase inhibitor. Otherwise, I had already tried to debunk this theory in previous posts on this site.

Just at face value cinnamon is a great anti-microbial with amazing anti-clotting and anti-inflammatory properties. Yes, cinnamon can lower LDL and triglycerides, while significantly raising HDL levels. However, cinnamon is perhaps also one of the best anti-oxidants in the entire class of spices.

What's more important is how cinnamon is able to prevent insulin resistance and sensitivity even in high-fructose diets. By mimicking insulin and slowing carbohydrate absorption it has a more than moderate anti-diabetic effects. What's not to like?

[Brian C.]

Hello adec, all's well on the Eastern Front.

There was some postings on this a while back from Biologist and Brooks I believe (though my memory is far from secure) that put me off taking the stuff. Didn't want to take a chance of putting the clock back, it's a protracted enough struggle as it is. "CoA reductase inhibitor" is a knee-jerk-reaction turn-off for me, no matter how mild the dose.

But on the other hand, I tolerate a little in a bun now and then

Do you know anything about berberine hydrochloride?

Brian.

[Biologist]

"Otherwise, I had already tried to debunk
this theory in previous posts on this site."
--adec

I must have missed them. Where are your posts on this matter, adec?

I'm sure you are giving bad advice. Cinnamon is a statin. It should be avoided -- particularly by people who have already been messed up by other statins.

On this forum I have showed via linking to published research papers that cinnamon is a statin and is used in industry to control (i.e., "selectively kill") bacteria in the gut of cattle, and is also used for the same purpose in the canning industry for extending shelf life.

Indeed, it evolved in the cinnamon plant to kill microbes and sicken or kill larger animals that would like to munch on it. It works. Most animals leave it alone. (Some don't learn.)

It's a statin. Don't do it.

On the other hand, sprinkling a little of it on oatmeal is probably no more harmful than sprinkling a little roach poison on one's oatmeal -- it will hardly be noticed.

I'll pass just the same.

Biologist

[vipergg22]

[quote="adec"][quote="Brian C."]Unfortunately cinnammon lowers cholesterol by a statin-like interference with the mevalonate pathway. I no longer take it.

Brian.[/quote]

Good morning Brian. Hope everything is well on your side of the pond. Yeah, I honestly don't know from where this overall conclusion comes. Do you have a link? Cinnamon oil *at best* is a benignly mild CoA reductase inhibitor. Otherwise, I had already tried to debunk this theory in previous posts on this site.

Just at face value cinnamon is a great anti-microbial with amazing anti-clotting and anti-inflammatory properties. Yes, cinnamon can lower LDL and triglycerides, while significantly raising HDL levels. However, cinnamon is perhaps also one of the best anti-oxidants in the entire class of spices.

What's more important is how cinnamon is able to prevent insulin resistance and sensitivity even in high-fructose diets. By mimicking insulin and slowing carbohydrate absorption it has a more than moderate anti-diabetic effects. What's not to like?[/quote]

I take cinnamon too , what is considered a safe amount per day ? I currently take 1000 mgs a day , basicaLLY 2 500 mg capsules with a meal . I too saw a 30 point drop in levels . Is 1000 enough and a safe level . I have seen no side effects from taking cinnamin either. Certainly seems a lot safer than a statins which basically destroyed the nerves in both feet after I took lipitor and zocor a few years ago . Never again .

[adec]

+++BIOLOGIST: Just realize that not only the cinnamon, but tocotrienols, aged garlic, oregano, rosemary, ginger, turmeric, curcumin, capsaicin, mustard, black pepper (and others) vary in metabolic degree as weak HMG-CoA reductase inhibitors and therefore possess lipidemic action.

However instead of like statins primarily *blocking* cholesterol synthesis and liver enzymes, these compounds mostly degrade or downregulate. This down/regulation is an important distinction, I believe. This is what makes high-dose statins so harmful, and these other compounds, not so much.

For instance, tocotrienols as the analogs to vitamin E increase farnesol along the mevalonate pathway, which then downregulates HMG-CoA. Tocotrienols are found most abundantly in many foods as essential oils of palm, barley, rye, rice and oat.

Obviously red rice yeast is nature's most powerful HMG-CoA reductase inhibitor, containing over nine such compounds. Perhaps tocotrienols would need to be standardized to farnesol to make the common dosage as dangerous as statins? I'm unsure of the answer. For instance, it takes over 2.4 grams of red yeast to manufacture just 8mg of lovastatin. Those active 3mg of mevinic acids are gives lovastatin the drug its powerful HMG-CoA reductase ability.

As you've already stated, natural foods such as cinnamon are added to livestock feed for their anti-microbial properties, which also includes corn, oregano, thyme, and cloves. Wouldn't you much rather see these natural alternatives being used in healthy livestock than indiscriminate antibiotics? Certainly an overabundance of microflora found in the animals' intestine would reduce nutrition. Especially in the presence of polysaccharides this could increase harmful bacteria and other pathogens. While cinnamon added to foods also acts as a strong preservative, the active anti-microbial component being cinnamaldehyde.

Ok. You want the second most dangerous compound threatening the mevalonate pathway? That would be bisphosphonates such as Fosamax, used most commonly to treat osteoporosis. These have been demonstrated to cause osteonecrosis, or bone death due to a loss of blood; and just recently, bisphosphonates have been found to cause an increase in heart valve damage and arterial fibrillation.


+++BRIAN: I know a little bit about berberine. It's derived from the barberry plant, and is a very powerful, safe, and effective anti-inflammatory in both the COX-2 and LOX-5 inhibitor class -- second only to the ursolic acid, as found most prevelently in the herb holy basil. I vaguely remember reading about it being used to lower blood sugar. Is this why you're asking about it?


+++VIPERGG22: There's a point of diminishing returns to cinnamon, likely anything above 250-500mg daily. Yes, I had written on this forum about the *slight* dangers of supplementing with household cinnamon. Whole cinnamon could potentially contain trace amounts of oil-based toxins and other volatile chemicals. You therefore have two options if there's any genuine concern a) purchase water-soluable cinnamon extracts, such as CinnulinPF or b) immerse cinnamon in boiling water and spoon off the excess lipids, let it dry and use. It's probably most safe and effective for lipid and blood sugar control to supplement with 500mg every other day... at least this is my opinion.

[Brian C.]

adec, I was asking about berberine because of this:

*http://www.nature.com/nm/journal/v10/n12/abs/nm1135.html;jsessionid=9795B21645EB1593C279DA808BC2BC5E

I have been taking berberine hydrochloride for a while to help keep my "cholesterol level" down in the high normal range since I don't fancy The Return Of The Xanthomas

Unfortunately, due to a protracted course of dental treatment I haven't seen my endoc doc for a while so have not had blood tests since taking the stuff.

I haven't come across anything regarding its lipid action other than that one article, just wondered if you had.

Brian.

[Biologist]

"However instead of like statins primarily *blocking*
cholesterol synthesis and liver enzymes, these
compounds mostly degrade or downregulate. This
down/regulation is an important distinction, I believe.
This is what makes high-dose statins so harmful,
and these other compounds, not so much."
--adec


adec,

You are slightly butchering biochemical definitions and distinctions. :wink: You are confusing terminologies to make inappropriate distinctions here and there -- part of them partly right, part of them simply wrong and inappropriate. Be that as it may, in short: Cinnamon has an identical action as a statin simply because it is a statin -- by DEFINITION. It is a HMG CoA Reductase Inhibitor (i.e, a statin).

It terminates the Mevalonate pathway. There are alternative means of reducing or increasing the concentration of the cholesterol molecule (and its various carrier types), but an HMG CoA reductase inhibitor is a HMG CoA reductase inhibitor. The more you take, the more its effect.

Statin damaged people are sensitized to statins and should not take them unnecessarily -- and certainly not therapeutically, which is what some people appear to be doing, like I did for a while until I ran into problems and subsequently did the research.

I like your interest in the subject. Keep studying.

Biologist

[adec]

Biologist, I never ask anyone to take me at my word. However, I do ask that we maintain a respectful dialog. I certainly apologize if my words were seen as an unnecessary slight. I share your passion adn skepticism; I also share your ire and frustration, but let's not misdirect it either.

Whole cinnamon is a compound with many functions and mechanisms of action due to various aldehydes, esters, and polymers. Just to clarify, perhaps whole cinnamon might share dual roles in terms as a downregulator and regulator, an inhibitor and a controller, blocker and degrader. Yet, I've searched and have not found a single paper demonstrating evidence of cinnamon, or its extracts, as a strong/broad HMG acyl-CoA reductase inhibitor in the statin class.

Statin is a specific term to a prescription class of drugs that effectively interfere or block HMG acyl-CoA to mevalonate. Otherwise we'd be calling magnesium a statin, as it too can *limit* this mevalonate formation to a large degree. What would we say here? I've seen magnesium mislabeled as a statin. There is an unknown almost corollary relationship between statins and magnesium. Magnesium, in fact, is required by the prevailing HMG-CoA limiting enzyme itself. I could leave it hanging right there, but instead will choose to clarify.

The rather recent distinction here is that magnesium acts more as a HMG-CoA controller and not an inhibitor. This too could be said for cinnamon. Which might suggest to avoid statin side effects, one most certainly must avoid magnesium -- perhaps cinnamon too. This most definitely is a new caveat. Meaning those being administered a statin would then be deficient in not only magnesium, but CoQ10. Or perhaps cinnamon has not been studied as extensively as the statin class of drugs. All such searches of cinnamon being a statin take me to this forum alone. Perhaps you can direct me to the proper place.

Otherwise, we can agree to disagree. Interestingly, one specific study demonstrated cinnamon ester's superiority in the beneficial elevation of high-density LDL over either the control or lovastatin. I also believe regulating blood sugar and decreasing insulin sensitivity are important primary factors in increasing longevity. Cinnamon in *moderation* can play an important role in this. Again, if one is inclined, avoid whole cinnamon and fat soluble cinnamon extract (Cinnamate) and supplement instead with water-soluble cinnamon extract (Cinnulin PF.)

[Darrell]

J Med Food. 2003 Fall;6(3):183-91.

Cinnamate supplementation enhances hepatic lipid metabolism and antioxidant defense systems in high cholesterol-fed rats.
Lee JS, Jeon SM, Park EM, Huh TL, Kwon OS, Lee MK, Choi MS.
Department of Food Science and Nutrition, Kyungpook National University, Daegu, Korea.

This study investigated the effect of cinnamate, a phenolic compound found in cinnamon bark and other plant materials, on lipid metabolism and antioxidant enzyme activities in rats fed a high cholesterol diet. Three groups of rats were given a diet containing 1 g of cholesterol/kg for 6 weeks. The control group only received the high cholesterol diet, whereas the other two groups received a diet supplemented with lovastatin or cinnamate (0.1 g/100 g of diet). The plasma high-density lipoprotein-cholesterol levels were significantly higher in the cinnamate group than in either the control or lovastatin groups, and the atherogenic index was significantly lower in rats with cinnamate supplementation. Supplementation with cinnamate resulted in significantly lower hepatic cholesterol and triglyceride levels. Accumulation of hepatic lipid droplets was higher in the control group than in the rats supplemented with either cinnamate or lovastatin. Hepatic 3-hydroxy-3-methylglutaryl CoA (HMG-CoA) reductase activity was significantly lower in the cinnamate group compared with the other groups, whereas only acyl-CoA:cholesterol acyltransferase activity was significantly lower in the lovastatin group compared with the control group. Cinnamate supplementation resulted in higher catalase and glutathione peroxidase activities, while hepatic thiobarbituric acid-reactive substances were significantly lower in both the cinnamate and lovastatin groups. The fecal acidic sterol was higher in the lovastatin group than in the control or cinnamate groups. These results suggest that dietary cinnamate inhibits hepatic HMG-CoA reductase activity, resulting in lower hepatic cholesterol content, and suppresses lipid peroxidation via enhancement of hepatic antioxidant enzyme activities.

PMID: 14585184 [PubMed - indexed for MEDLINE]

[adec]

Darrell, this was the lone study in question. I was hoping someone had something more than just the abstract. However, it used cinnamon ester, and further states these results only "*suggest* that dietary cinnamate inhibits hepatic HMG-CoA reductase activity." It neither tells the degree of inhibition, the metabolic pathway, or the main mechanism of action. This is an important omission. We also don't know the effect Cinnamate has on fluctuating CoQ10 levels.

The study does, however, strongly suggest that cinnamate actually inhibits HMG-CoA via the pentose-phosphate pathway, being as it "resulted in higher catalase and glutathione peroxidase activities." This might in part secure a role as a more effective anti-oxidant vs. statins.

We also might regard fat-soluble cinnamon esters and aldehydes (such as cinnamate and cinnamonaldehyde) as better regulators of LDL and Triglycerides, while the water-soluble cinnamon polymers and polyphenols act more as insulin mimetics and blood glucose regulators. We most definitely know cinnamonaldehyde -- not cinnamate -- comprises a large percentage (80-90%) of the essential oils of cinnamon bark.

I was looking for a definitive study or single paper *conclusively "demonstrating evidence of cinnamon, or its extracts, as a strong/broad HMG acyl-CoA reductase inhibitor in the statin class." As we've plainly discovered, prescription statins are engineered to devastate everything in the melovanate pathway. I certainly have found copious studies regarding common tocotrienols (or analogs to vitamin E) and magnesium as a fairly strong inhibitors of HMG-CoA reductase via the mevalonate pathway -- while aged garlic inhibits HMG-CoA via the acetate pathway, and perhaps cinnamon esters via the the pentose-phosphate pathway. (Meaning the degree to which foods and supplements vary as HMG-CoA reductase inhibitors is bound by many complex and unique factors.)

Just to demonstrate the dietary ubiquity of tocotrienols, and the means necessary toward thorough compliance of anything *non*-HMG-CoA reductase inhibitor.

Supplementwatch.com: Tocotrienol
*http://www.supplementwatch.com/suplib/supplement.asp?DocId=2544
......................................................................................................................................
Tocotrienols can be found in oils and fats (e.g. rice bran, barley),
vegetables and grains (e.g. wheat, barley, rice), fruits (e.g. avocados,
blueberries, olives), nuts and seeds (e.g. almonds, coconut, annatto), and
meats and eggs. The most common sources of tocotrienols in the supplement
industry are rice, palm, and annatto. Rice and palm tocotrienols contain
25-50% of tocopherols, most of which is alpha-tocopherol. Annatto, on the
other hand, contains only gamma- and delta-tocotrienol, is tocopherol-free,
and therefore the best source of the form of tocotrienols (desmethyl) that
are potent in lipid lowering and cardiovascular support.
Here's are two studies on tocotrienols giving the actual degree of
inhibition, and describing the mode of action.

[adec]

+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==
Tocotrienols regulate cholesterol production in mammalian cells by post-
transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A
reductase
RA Parker, BC Pearce, RW Clark, DA Gordon and JJ Wright
Department of Metabolic Diseases, Bristol-Myers Squibb Pharmaceutical
Research Institute, Princeton, New Jersey 08543.

Tocotrienols are natural farnesylated analogues of tocopherols which
decrease hepatic cholesterol production and reduce plasma cholesterol levels
in animals. For several cultured cell types, incubation with
gamma-tocotrienol inhibited the rate of [14C]acetate but not [3H] mevalonate
incorporation into cholesterol in a concentration- and time- dependent
manner, with 50% inhibition at approximately 2 microM and maximum
approximately 80% inhibition observed within 6 h in HepG2 cells.
3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase total activity and
protein levels assayed by Western blot were reduced concomitantly with the
decrease in cholesterol synthesis. In HepG2 cells, gamma-tocotrienol
suppressed reductase despite strong blockade by inhibitors at several steps
in the pathway, suggesting that isoprenoid flux is not required for the
regulatory effect. HMG-CoA reductase protein synthesis rate was moderately
diminished (57% of control), while the degradation rate was increased
2.4-fold versus control (t1/2 declined from 3.73 to 1.59 h) as judged by
[35S]methionine pulse-chase/immunoprecipitation analysis of HepG2 cells
treated with 10 microM gamma-tocotrienol. Under these conditions, the
decrease in reductase protein levels greatly exceeded the minor decrease in
mRNA (23 versus 76% of control, respectively), and the low density
lipoprotein receptor protein was augmented. In contrast, 25-
hydroxycholesterol strongly cosuppressed HMG-CoA reductase protein and mRNA
levels and the low density lipoprotein receptor protein. Thus, tocotrienols
influence the mevalonate pathway in mammalian cells by post-transcriptional
suppression of HMG-CoA reductase, and appear to specifically modulate the
intracellular mechanism for controlled degradation of the reductase protein,
an activity that mirrors the actions of the putative non-sterol isoprenoid
regulators derived from mevalonate.
+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==



+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==
Title: Inhibitors of cholesterol biosynthesis. 2. Hypocholesterolemic
and antioxidant activities of benzopyran and tetrahydronaphthalene analogues
of the tocotrienols.
Author: Pearce, B C : Parker, R A : Deason, M E : Dischino, D D :
Gillespie, E : Qureshi, A A : Volk, K : Wright, J J
Citation: J-Med-Chem. 1994 Feb 18; 37(4): 526-41
Abstract: Tocotrienols exhibit antioxidant and
cholesterol-biosynthesis-inhibitory activities and may be of value as
antiatherosclerotic agents. The mechanism of their hypolipidemic action
involves posttranscriptional suppression of HMG-CoA reductase (HMGR) in a
manner mimicking the action of putative non-sterol feedback inhibitors. The
in vitro cholesterol-biosynthesis-inhibitory and HMGR-suppressive activities
in HepG2 cells of an expanded series of benzopyran and tetrahydronaphthalene
isosteres and the hypocholesterolemic activity of selected compounds
assessed in orally dosed chickens are presented. Preliminary antioxidant
data of these compounds have been obtained using cyclic voltammetry and
Cu-induced LDL oxidation assays. The farnesyl side chain and the
methyl/hydroxy substitution pattern of gamma-tocotrienol deliver a high
level of HMGR suppression, unsurpassed by synthetic analogues of the present
study. In orally dosed chickens, 8-bromotocotrienol (4o),
2-desmethyltocotrienol (4t), and the tetrahydronaphthalene derivative 35
exhibit a greater degree of LDL cholesterol lowering than the natural
tocotrienols.
+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==+==

[adec]

[v] Rosanoff, Andrea. Seelig, Mildred. Comparison of Mechanism and Functional Effects of Magnesium and Statin Pharmaceuticals. Department of Physiology and Pharmacology, State University of New York, Downstate Medical Center, Brooklyn (M.S.) Since Mg2+-ATP is the controlling factor for the rate-limiting enzyme in the cholesterol biosynthesis sequence that is targeted by the statin pharmaceutical drugs, comparison of the effects of Mg2+ on lipoproteins with those of the statin drugs is warranted. Formation of cholesterol in blood, as well as of cholesterol required in hormone synthesis, and membrane maintenance, is achieved in a series of enzymatic reactions that convert HMG-CoA to cholesterol. The rate-limiting reaction of this pathway is the enzymatic conversion of HMG CoA to mevalonate via HMG CoA. The statins and Mg inhibit that enzyme. Large trials have consistently shown that statins, taken by subjects with high LDL-cholesterol (LDL-C) values, lower its blood levels 35 to 65%. They also reduce the incidence of heart attacks, angina and other nonfatal cardiac events, as well as cardiac, stroke, and total mortality. These effects of statins derive less from their lowering of LDL-C than from their reduction of mevalonate formation which improves endothelial function, inhibits proliferation and migration of vascular smooth muscle cells and macrophages, promotes plaque stabilization and regression, and reduces inflammation, Mg has effects that parallel those of statins. For example, the enzyme that deactivates HMG-CoA Reductase requires Mg, making Mg a Reductase controller rather than inhibitor. Mg is also necessary for the activity of lecithin cholesterol acyl transferase (LCAT), which lowers LDL-C and triglyceride levels and raises HDL-C levels. Desaturase is another Mg-dependent enzyme involved in lipid metabolism which statins do not directly affect. Desaturase catalyzes the first step in conversion of essential fatty acids (omega-3 linoleic acid and omega-6 linolenic acid) into prostaglandins, important in cardiovascular and overall health. Mg at optimal cellular concentration is well accepted as a natural calcium channel blocker. *More recent work shows that Mg also acts as a statin.*

[cjbrooksjc]

I am reminded of a Charlie Brown cartoon in which two of Charlie's friends, staring at the clouds, tell Charlie they see, (and I paraphrase) 1. the outline of Louis Pasteur swilling about a formulation of a cure for Anthrax, and 2. Pontius Pilate washing his hands following Christ's delivery to crusifiction, and Charlie says: "I was going to say I saw a horsey and a duckey, but I've changed my mind."

That said, I don't know what I can add to this rather cumbersome dialog, but when I got off the statins, a family friend (an osteopathic Dr.) ran a magnesium absorption test on me, and I failed to the point of fascination. I was wondering if that simple result made any sense or had any potential value as data owing to the fact that I had been taking, up to that day and for the past three years, 40 Mg of Zocor. Any idea why that depletion should be evidenced? My diet, BTW, is and was quite normal: meat, vegs, eggs, grain, etc.

Regards,

Brooks

[Biologist]

That was good, Brooks

On the magnesium thing, interesting. It's on the radar now.

I am just getting caught up at work and headed out for a short vacation for a few days. Looks promising, but then, that's what I thought the last few times...

*http://www.snoopy.com/comics/peanuts/greatpumpkin/images/scene_3_large.gif

(The Lucy factor)

I hope to post a few more thoughts re cinnamin in this tread before I leave. If not, when I get back maybe.

Biologist

[Biologist]

Several points:

There has been some apparent confusion about the definition of a statin in this thread. I believe the first paragraph here is a reasonable definition and certainly one acceptable to Big Pharma who either wrote the section on statins or keep it regularly edited to their liking (it sure reads like it):

*http://en.wikipedia.org/wiki/Statin

The "take home message" here is that term "Statin" and the term "HMG-CoA reductase inhibitor" are considered synonymous.

I would not have been surprised if there were no studies showing cinnamon to be a statin. (Darrell made a good find.) And I'm sure not surprised that it is not advertised or commonly known as such. Who profits? Not drug companies for sure. Example: "Hey, you know, you can go buy several thousand dollars worth of statins at Sam's Club for less than a hundred bucks." That little factoid would cost "the economy" several tens of billions of dollars every year in lost Pharma revenues. Also the "alternative medicine" crowd is sure not eager to advertise the fact that their answer to the evil stains is in fact a statin. In fact, I'm not much interested in the word getting out. Gees. It might as well be in the water then for sure. We would be a whole world of mental and physical cripples inside of a decade -- now that could really hurt an economy!

I have no reason to believe that the statin activity in red yeast rice is more or less powerful than cinnamon on an ounce for ounce basis. It is almost a meaningless issue without factoring in the dosages. I know of an atypically mentally and physically fit physician who had serious problems with 5 mg. of Lipitor. Would he have been better off with a hundred time more (i.e., 500 mg.) of cinnamon? I don't know. Maybe. However, I have never heard of him recommending cinnamon while he has suggested numerous other alternatives, if necessary, for some people, in some cases.

Cinnamon is as wholesome and American as Mom's Apple Pie? (Sorry, Brian). Hell, it's even IN Mom's Apple Pie! There are a lot of places on the web (and other places) that recommend cinnamon for the reasons adec suggests. However, for people who have had obvious problems from statins, I would recommend keeping cinnamon consumption to a minimum -- apple pie excepted of course.

adec, you still get credit for the best post I've read in years. The vitamin D video was ahead of its time by a minimum of six months, which is an eon in today's world. I sent it to a lot of people and an organization or two. Big hit.

Biologist

[cjbrooksjc]

Biologist: I particularly liked this description of Zocor: Simvastatin is a synthetic derivate of a fermentation product. Who in their right minds would take something with that moniker? "Synthetic Deviate". I love it! Aside from that piece of whimsy, it was a great article and a url I will add to my library. And the Vitamin D thing? Yes, it was one of the most informative and illuminating things I've read/seen in many years. I now take Vit D daily as a result. Thanks for the link. Have a restful vacation.

Regards,

Brooks

[Brian C.]

Biologist, please don't say "apple pie"

Not lunch-time yet.....




Brian.