27 May 2012

Saturated fats, cholesterol, heart disease

By my research, the "saturated fat causes heart disease" debate appears to go back to the 1950's when someone selected the data from 6 countries to show that fat consumption was linked to heart disease rates.  As the story goes, he excluded the data from 16 other countries that was available, which would have make this link all but disappear.  Many other scientists were quite skeptical of his views at this time.  Of course the unsaturated fat industries such as corn jumped on these findings to forever impress into peoples minds that saturated fats are "bad" fats.  Mind you, corn can be fattening, while coconut oil - largely a saturated fat - can assist with losing weight.

Some articles and blogs on saturated fats
http://thehealthyadvocate.com/2012/02/24/coconut-oil-increases-cholesterol-yet-is-still-healthy-for-your-heart/
http://health.newsvine.com/_news/2010/05/30/4440758-what-if-bad-fat-isnt-so-bad
http://www.drbriffa.com/2011/09/21/huge-study-finds-gaping-holes-in-the-cholesterol-hypothesis/

What do I think of cholesterol, heart disease, and saturated fats?
Is LDL really that bad for you?  And does a high LDL really ensure you heart disease in the future?  Should you take statins to control high cholesterol?  It is not well known that statins inhibit the bodies ability to produce CoQ10.  For those that dont know, CoQ10 is a critical antioxidant for heart health.  If the body reduces production, then you are potentially creating new heart problems.

My current view is that:
  • A higher than normal LDL is not necessarily bad for you, so long as your LDL:HDL ratio is acceptable. Obviously this is within limits, but I havent seen research to know what those limits should be.
  • LDL cholesterol is most likely not dangerous (lets face it, without enough LDL in your body, you are going to die as you require it to perform some basic functions including the synthesis of vitamin D).  My view is that LDL becomes dangerous when it is oxidised, and this is related to a diet containing processed foods and sugars, or consuming overcooked cholesterol (for example, overcooking the yolk of the egg). 
  • Published articles also indicate that LDL particle size has a part to play in whether the LDL is small enough to be stuck in your arteries.  A highly processed diet and sugars also probably play a large part in this. 
So to my way of thinking, the solution is not to look at lowering LDL as the highest priority (although it is important to ensure LDL:HDL ratios are in check), but to significantly reduce intake pf processed foods and sugars.

If the issue of concern is heart disease, then once again, based on what I have read, these are the more important indicators of heart disease:

  • Oxidative Stress which may lead to higher CRP (c-reactive protein) levels. Higher CRP has been associated with CHD. CRP is a marker in the blood that indicates low level inflammation.  You can have your CRP tested. 
  • Oxidized LDL
  • LDL particle sizes
  • Level of triglycerides in the blood
  • Diabetes is a risk factor also, possibly due to the difference in particle sizes in people with diabetes.
So is coconut oil good for you then?
As a side topic, is coconut oil really bad for you?  As I have been touting for a long while now, if you want to lose weight, coconut oil is a fantastic way to do it.

Lipids. 2009 Jul;44(7):593-601. Epub 2009 May 13. PMID: 19437058
Article Published Date : Jul 01, 2009
http://www.greenmedinfo.com/article/dietary-coconut-oil-elevates-hdl-and-reduces-abdominal-obesity-women
The effects of dietary supplementation with coconut oil on the biochemical and anthropometric profiles of women presenting waist circumferences (WC) >88 cm (abdominal obesity) were investigated. The randomised, double-blind, clinical trial involved 40 women aged 20-40 years. Groups received daily dietary supplements comprising 30 mL of either soy bean oil (group S; n = 20) or coconut oil (group C; n = 20) over a 12-week period, during which all subjects were instructed to follow a balanced hypocaloric diet and to walk for 50 min per day. Data were collected 1 week before (T1) and 1 week after (T2) dietary intervention. Energy intake and amount of carbohydrate ingested by both groups diminished over the trial, whereas the consumption of protein and fibre increased and lipid ingestion remained unchanged. At T1 there were no differences in biochemical or anthropometric characteristics between the groups, whereas at T2 group C presented a higher level of HDL (48.7 +/- 2.4 vs. 45.00 +/- 5.6; P = 0.01) and a lower LDL:HDL ratio (2.41 +/- 0.8 vs. 3.1 +/- 0.8; P = 0.04). Reductions in BMI were observed in both groups at T2 (P < 0.05), but only group C exhibited a reduction in WC (P = 0.005). Group S presented an increase (P < 0.05) in total cholesterol, LDL and LDL:HDL ratio, whilst HDL diminished (P = 0.03). Such alterations were not observed in group C. It appears that dietetic supplementation with coconut oil does not cause dyslipidemia and seems to promote a reduction in abdominal obesity

Effects of dietary coconut oil on the biochemical and anthropometric profiles of women presenting abdominal obesity.


What does the web say?



What do the studies say?



http://archinte.jamanetwork.com/article.aspx?volume=169&issue=7&page=659
Higher intake of α-linolenic acid, eggs, meat, milk, polyunsaturated fatty acids, saturated fatty acids, total fat, and ascorbic acid (vitamin C) and vitamin E supplements and prudent and western diet patterns were not significantly associated with CHD (Table 2). Among studies of higher methodologic quality, prudent (RR, 0.73 [95% CI, 0.62-0.83]) and western (1.55 [1.27-1.83]) diet patterns were each associated with CHD. In keeping with previous information, fish intake was protective against fatal CHD (RR, 0.83 [95% CI, 0.71-0.94]), but marine ω-3 fatty acids (0.88 [0.66-1.11]) and α-linolenic acid (0.98 [0.60-1.36]) were not.

http://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstract
Results: During 5–23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. The pooled relative risk estimates that compared extreme quantiles of saturated fat intake were 1.07 (95% CI: 0.96, 1.19; P = 0.22) for CHD, 0.81 (95% CI: 0.62, 1.05; P = 0.11) for stroke, and 1.00 (95% CI: 0.89, 1.11; P = 0.95) for CVD. Consideration of age, sex, and study quality did not change the results.
Conclusions: A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat


http://www.ncbi.nlm.nih.gov/pubmed/15585208

OBJECTIVE:

Increases in the inflammatory marker C-reactive protein (CRP) have been associated with a higher risk of incident coronary heart disease (CHD). The causes of increased CRP, however, are not completely understood. Studies suggest that oxidative stress may have pro-inflammatory effects, but data on the relationship between oxidative stress and CRP in healthy persons is sparse.

METHODS AND RESULTS:

We conducted a cross-sectional study of oxidative stress markers and high sensitivity CRP (hsCRP) among 126 adults without CHD. Markers of oxidative stress included the free oxygen radical test (FORT), which reflects levels of organic hydroperoxides, and the redox potential of the reduced glutathione/glutathione disulfide couple, (Eh) GSH/GSSG. In a linear regression model that adjusted for age, sex, body mass index, and other potential hsCRP determinants, the FORT was positively associated with log-transformed hsCRP and explained 14% of log-transformed hsCRP variance (P < 0.001). In contrast, (Eh) GSH/GSSG showed little association with hsCRP.

CONCLUSIONS:

Among adults free of CHD, oxidative stress, as measured by the FORT, is significantly associated with higher hsCRP levels, independent of BMI and other CRP determinants. This result suggests that oxidative stress may be a determinant of CRP levels and promote pro-atherosclerotic inflammatory processes at the earliest stages of CHD development.


http://www.ncbi.nlm.nih.gov/pubmed/21697499

BACKGROUND:

Oxidative stress plays a critical role in the initiation and progression of atherosclerosis. Oxidized LDL (oxLDL) is a marker of oxidative stress. We prospectively investigated whether increased serum oxLDL concentrations are associated with incident coronary heart disease (CHD).

METHODS:

We conducted a prospective population-based case-cohort study within the MONICA/KORA Augsburg studies. Serum oxLDL concentrations were measured in 333 case individuals with incident CHD and in 1727 noncase individuals selected from a source population of 9300 middle-aged, healthy men and women. The mean (SD) follow-up time was 10.8 (4.6) years.

RESULTS:

Baseline oxLDL concentrations were higher in case individuals than in noncase individuals (P < 0.001). After adjustment for age, sex, survey, smoking status, systolic blood pressure, physical activity, diabetes, body mass index, parental history of myocardial infarction, and alcohol consumption, the hazard ratio (HR) for comparing the first and third tertiles was 1.87 (95% CI, 1.33-2.64; P < 0.001). Additional adjustment for lipid parameters, inflammatory markers, and markers of endothelial dysfunction attenuated the association (HR, 1.29; 95% CI, 0.88-1.89; P = 0.087). We observed no significant interactions between oxLDL and sex or being overweight.

CONCLUSIONS:

Increased oxLDL concentrations were associated with an increased risk for incident CHD. Nevertheless, because this effect became nonsignificant after adjustment for covariates, particularly the ratio of total cholesterol to HDL cholesterol, it may be mediated primarily by lipid parameters. Further studies are warranted to clarify this issue.


http://www.ncbi.nlm.nih.gov/pubmed/22586500

Abstract

The aim of this study was to investigate the influencing factors that characterize low density lipoprotein (LDL) phenotype and the levels of LDL particle size in healthy Korean women. In 57 healthy Korean women (mean age, 57.4 ± 13.1 yrs), anthropometric and biochemical parameters such as lipid profiles and LDL particle size were measured. Dietary intake was estimated by a developed semi-quantitative food frequency questionnaire. The study subjects were divided into two groups: LDL phenotype A (mean size: 269.7Å, n = 44) and LDL phenotype B (mean size: 248.2Å, n = 13). Basic characteristics were not significantly different between the two groups. The phenotype B group had a higher body mass index, higher serum levels of triglyceride, total-cholesterol, LDL-cholesterol, apolipoprotein (apo)B, and apoCIII but lower levels of high density lipoprotein (HDL)-cholesterol and LDL particle size than those of the phenotype A group. LDL particle size was negatively correlated with serum levels of triglyceride (r = -0.732, P < 0.001), total-cholesterol, apoB, and apoCIII, as well as carbohydrate intake (%En) and positively correlated with serum levels of HDL-cholesterol and ApoA1 and fat intake (%En). A stepwise multiple linear regression analysis revealed that carbohydrate intake (%En) and serum triglyceride levels were the primary factors influencing LDL particle size (P < 0.001, R(2) = 0.577). This result confirmed that LDL particle size was closely correlated with circulating triglycerides and demonstrated that particle size is significantly associated with dietary carbohydrate in Korean women.

http://www.ncbi.nlm.nih.gov/pubmed/22584085

BACKGROUND:

A higher prevalence of coronary heart disease (CHD) in people with diabetes. We investigated the high-density lipoprotein (HDL) subclass profiles and alterations of particle size in CHD patients with diabetes or without diabetes.

METHODS:

Plasma HDL subclasses were quantified in CHD by 1-dimensional gel electrophoresis coupled with immunodetection.

RESULTS:

Although the particle size of HDL tend to small, the mean levels of low density lipoprotein cholesterol(LDL-C) and total cholesterol (TC) have achieved normal or desirable for CHD patients with or without diabetes who administered statins therapy. Fasting plasma glucose (FPG), triglyceride (TG), TC, LDL-C concentrations, and HDL3 (HDL3b and 3a) contents along with Gensini Score were significantly higher; but those of HDL-C, HDL2b+prebeta2, and HDL2a were significantly lower in CHD patients with diabetes versus CHD patients without diabetes; The prebeta1-HDL contents did not differ significantly between these groups. Multivariate regression analysis revealed that Gensini Score was significantly and independently predicted by HDL2a, and HDL2b+prebeta2.

CONCLUSIONS:

The abnormality of HDL subpopulations distribution and particle size may contribute to CHD risk in diabetes patients. The HDL subclasses distribution may help in severity of coronary artery and risk stratification, especially in CHD patients with therapeutic LDL, TG and HDL levels.

http://www.ajconline.org/article/S0002-9149(00)00956-5/abstract
Low-density lipoprotein particle size, triglycerides, and high-density lipoprotein cholesterol as risk factors for coronary heart disease in older Japanese-American men
Decreased low-density lipoprotein (LDL) particle size is associated with coronary heart disease (CHD) risk among middle-aged Caucasian populations, and has been consistently correlated with increased plasma levels of triglyceride and decreased levels of high-density lipoprotein (HDL) cholesterol. This study examines whether these risk factors predict CHD among older Japanese-American men. With use of the Honolulu Heart Program Lipoprotein Exam 3 (1980 to 1982) as baseline, and 12-year follow-up for CHD events, a nested, case-control study was designed. One hundred forty-five incident CHD cases were identified and matched to 2 controls each. LDL particle diameter (size) was determined by gradient gel electrophoresis. A 10-angstrom (Å) decrease in LDL size at baseline was associated with increased risk of incident CHD (relative risk 1.28, 95% confidence interval 1.01 to 1.63). After adjustment for baseline risk factors, the LDL size association was no longer statistically significant (relative risk 1.13, 95% confidence interval 0.86 to 1.49). When principal components analysis was used to define a composite variable for LDL size, triglycerides, and HDL cholesterol, this component predicted CHD independent of smoking, alcohol consumption, physical activity, body mass index, hypertension, diabetes, and β-blocker use (p <0.01). Therefore, this prospective analysis of data from older, Japanese-American men demonstrated that decreased LDL size is a univariate predictor of incident CHD, and that a composite risk factor of LDL size, triglyceride, and HDL cholesterol was a risk factor for CHD independent of other risk factors.

Potential Solutions to Heart Disease
A study published in the Journal of Nutrition (2004) showed that walnuts had a beneficial effect on cholesterol levels and C-reactive protein (CRP), which is an inflammation marker strongly associated with atherosclerosis and artery disease