The Good Fats

the problem with MCT oil is it adversely affects the chol/HDL ratio- in fact, historically MCT oil was used to treat hypertriglyceridemia, but was scrapped because of the increase in bad cholesterol- marketing MCT as brain fuel seems silly- the amount on the market is slim to none, with no retarding brain function- when i was a kid, the cliche was that fish is brain food- in terms of axonal support (which is not brain food but brain infrastructure), i would choose omega 3s over MCT any day

May I suggest you read P. Hujoel   Dietary Carbohydrates and Dental-Systemic Diseases

and statins and vitamin D The diet-cholesterol-heart hypothesis dominated medical thinking for the latter half of the 20th century and it still persists. The diet component has so many inconsistencies that it is unsustainable. It continues in popular folklore and government dietary policies but it seems to have been quietly dropped by most cholesterol-heart researchers.

The original cholesterol-heart studies were undisputed at the time but the evidence is now not quite so clear. 

If you would like to keep up to date with current thinking them may I suggest you follow a blog like Whole Health Source or The Heart Scan Blog Nephropal also tries to explain the science in simple terms.

May I suggest you read M. Brown http://www.sciencemag.org/cgi/content/summary/272/5262/629

The fact that oxidized LDL is a primary etiological progression of atherosclerosis dominated medical thinking for the latter half of the 20th century and it still persists. The only real question is what drives the oxidation and what inhibits it. Any dietary factor which chronically raises circulating LDL will logiucally drive the equilibrium of oxidizing LDL forward.  The use of MCT oil in attenuating heart disease was found to raise LDL and seems to have been quietly dropped by most cholesterol-heart reasearchers.

If you would like to keep up to date with current research then may I suggest you follow the ALLHAT trial which tries to explain the science in simple terms

http://www.ncbi.nlm.nih.gov/pubmed/8722437

Effect of Intensive Versus Standard Lipid-Lowering Treatment With Atorvastatin on the Progression of Calcified Coronary Atherosclerosis Over 12 Months

We did not observe a relationship between on-treatment LDL cholesterol levels and the progression of calcified coronary atherosclerosis. Over a period of 12 months, intensive atorvastatin therapy was unable to attenuate CAC progression compared with standard atorvastatin therapy

from U of Texas MC molecular genetics dept (so no horse in the 'diet debate' race):

evidence for the causative role of LDL comes from 3 sources. 1- experimental: animals with low levels of LDL have no atheroscerosis, and manipulations that raise LDL universally cause the disease. 2- epidemiologic: human populations with low LDL levels have very little atherosclerosis; the disease increases in proportion to LDL in all populations studied. 3- genetic: mutations that impair the receptor-mediated removal of LDL from plasma cause fulminant atheroscerosis.  The final (therapeutic) line of evidence has been supplied by 3 clinical trials.

http://www.sciencemag.org/cgi/content/summary/272/5262/629

The Diet-Heart Hypothesis: Stuck at the Starting Gate

The Diet-Heart Hypothesis: A Little Perspective

Cholesterol and mortality: 30 years of follow-up from the Framingham study. 

This Framingham study shows the significant relationship between high serum cholesterol and reduced life expectancy applies only to young men.

Influence of Pravastatin and Plasma Lipids on Clinical Events in the West of Scotland Coronary Prevention Study (WOSCOPS) it is clear from this study that the clinical benefit bears no relationship to cholesterol lowering. The author suggest statins might be acting in ways other than cholesterol lowering.

Prevalence of coronary heart disease in the Framingham Offspring Study: role of lipoprotein cholesterols

This Framingham study shows the prevalence of coronary heart disease in men was strongly associated with LDL

The benefits associated with cholesterol reduction may not outweigh the risks in all patients with hypercholesterolemia. Cholesterol-lowering interventions should be recommended with caution in patients at increased risk of cancer, stroke, and depression".

Here is a Pubmed list of abstracts about low or lowered cholesterol health implications -

well, if by "interventions" you mean drugs, i agree- i am not an advocate for the pharmaceutical industry- however, diet and exercise both lower cholesterol and are preventative interventions for cancer and stroke- as for depression, i can't verify, but i'm gonna get a bottle of whiskey and drown my sorrows (ETOH raises HDL)

MRFIT Mortality

total mortality is nearly as high at low cholesterol levels as at high cholesterol levels

Alzheimer's and Ketones at the end of this blog Peter has an interesting comment on the efffect of MCT's on appetite in diabetic rats. 

The benefit of medium-chain triglyceride therapy on the cardiac function

Prolonged exposure to high dietary lipids is not associated with lipotoxicity in heart failure.

Medium-chain fatty acids as metabolic therapy in cardiac disease.

Hello to everyone on the above exchanges and thanks.  Are any of you Type 1?

Can you please simplify a little for me.?I have been reading and reading and reading and so now feel thoroughly confused, I am running HIGH HDL, LOW triglycerides and moderately hign LDL and have ,besides being a little lax in the exercise department, been following Richard K. Bernstein for the past year. I am being scored in metric scale (hello fellow Canucks) and the LDL went from 4.5 to 5 in a period of high stress, low veggie consumption and falling exercise, also the past year.

I am reading Gary Taubes and Sally Fallon and they all seem to be encouraging (along with Bernstein) saturated fats and reassuring that LDL is not dangerous, but VLDL is. This is not differntiated in the tests done. Do you all have this separated on your test results.

Some more thoughts on this and who did what to bring down LDL....sardines and almonds sound good to me. What else? I am now much less stressed and have been walking/running atleast a mile a day, lifting some weights and purtsuing an interest in yoga....soon to come dance class.....for the past 2-3 months.

Thanks to all of you; I find this site so informative and human scale. I look forward to hearing your experience and thoughts.

Jane

I am T2 (2 oral meds) w/ T2 complications (blind 1 eye; kidney flares; polyneur-opathy, coagulation issues, etc.) - Male, A: 63, USA, northern European caucasian) - The only good news is my 7/1/09 Hba1c was 5.1, as I am essentially a vegan (ugh).

I am swapping (O6,trans,sat) fatlaced-calories for yrs: An inelegant, BUT BALANCED, equation.)

I suppose (I'm not a doctor) you are right that it is said that lipids, BY & UNTO THEMSELVES, may not be the "complete, all explanatory bogey" once believed. BUT - "inflammation" certainly is a huge problem, if I understand any of this even a little. 

SO - anything you can do to "interrupt the cascade" that inflammation plays such an integral role in has got to be a good idea, no? And with O6s being simply everywhere in our Western diets (they're cheap, tasty & texture-builders), they are thus the ez, go-to target for all of us to nail in getting our "inflammation index number" (so to speak) dialed down, waay down.

Sorry I can't put it any better. Undoubtedly, someone will (is there an RDorCNorCDE in the house?)

Thank you for such a rapid response. Where does one find the 06 inflammatory villains? I am not certain that I am eating many of those with the high level of vegetables that I consume. Minimal dairy, no junk (food) in the house ,water,water,water,limited fruits,organic pasture fed meats and eggs,no wheat,daily sardines or herring. Where in there is the omega 6? Yes, there is a dietitian in the house,not easily available.

Thanks again for your interest and help.

Jane

You're right. I don't see any O6s (or fats for that matter) in your listings, but I'm no CN, RD, MD, etc. The oil in the sardines, etc. assumed to be olive oil. Are you getting focused, expert advice (eg, endocrinologist) Remember: sunflower, safflower, corn oil are not as good as olive oil, although I don't see these in anything you listed. (Anything left out?) Perhaps letting a diabetologist-endocrinologist take a shot will help. My problem is partially explained by genomics, so I bring issues to the dinner table even as I sit down to it. Maybe you too.

Omega-6 Fat News & Commentary
Research News by Evelyn Tribole, MS, RD

this website has a useful gadget for working out your omega 6 intake as well as lots of up to date research on the adverse effects of omega 6 on heart and brain health.

One thing I learnt recently about canned fish in oil is that it leaches the omega 3 from the fish into the canning oil and so if you then pour the oil away before eating the fish you are pouring away the omega 3 but consuming higher amounts of omega 6 that have infiltrated into the fish flesh. So only buy fish canned in water or olive oil and then make sure you consume the olive oil. 

Vegetables contain omega-6 oils. I don't think the amounts for most of them are large enough to worry about, but you could consult the USDA nutritional site to see how many are in the veggies you eat.

Nuts and seeds also contain some omega-6 oils in addition to omega-3, saturated, etc.

Even "monounsaturated" oils like olive oil contain some of the other fats.

Forgot to address your ? re 'VLDL' testing. In USA (maybe you too) a test-panel called a "VAP" will get you a 'VLDL' figure (along w/ other lipid metrics, eg: lipid particle size) - Not ez to get done due to cost, BUT has been instrumental in helping me scope out where my problems lay in the various lipid 'components', which for me turned out to be plural (eg: Lpa, Lpa(2), VLDL3, apoB, B/AB/A sizing.)