The Fuhrman/McDougall diet are no guarantee that you will not have a heart attack or cardio disease.Dolores was 95% or better compliant and she still had a heart attack and so did this person from the McDougall forum.
I have diabetes which I controlled pretty well with diet though my numbers were still higher than "normal". I wouldn't take medicine. also had high blood pressure and didn't want to take medicine but finally did. supposedly it all contributed (though I've been a vegetarian for 26 years) and I had a heart attack Jan. 23 with blockage at 70% to 100%. had bypass surgery Jan. 25. at the time I was doing good on the McD plan (having lost the weight a few years ago) and no added oil.
I am, at least temporarily, taking med for blood pressure and cholesterol though the latter wasn't high. nothing for diabetes but I eat less now and no oil so my morning fasting tests are good, about 113.
I assume I would still fail the glucose test like I did years ago"
It looks to me like insulin (hyperinsulinemia) is the key! I found that idea years ago from Dr. Rosedale article and everything I later learned has corroborated that original idea.
High insulin level is also, by itself, a contributory factor for hypertension and direct stimulator of arterial plaque growth.
High insulin level together with insulin resistance resets the peroxide signalling at a higher level which then causes mitochondrial damage which then causes the metabolic yield to fall exacerbating the damage due to overfeeding and to the peroxides and free radical residuals.
There are immediate consequences of hyperinsulinemia, such as above mentioned hypertension. Also slowed down ketone production which forces heart muscle and brain to utilize more glucose than they really should (note: amyloid plaque is glucose metabolic residual).
There are also long term negative implications that have to do with the above-mentioned peroxides and free radical damage to the cells and mitochondria that mimic aging. There is a reason insulin is sometimes called "death hormone". The reason is because bacteria use insulin signalling to trigger apoptosis.
This is the main reason why you can be thin and suffer a heart attack, or you can be fat and never get it!
Obesity is not always indicative of hyperinsulinemia and being thin is not an indication of a lack of hyperinsulinemia.
If you eat a lot of carbs, especially together with equal amount of fat, more than your body really needs then it fuels insulin resistance and hyperinsulinemia. If you keep snacking frequently with carbs then it also maintains a state of chronically raised insulin.
I believe the only safe way of eating a high carbohydrate diet is to eat only once a day like Kitavans, so that the body can maintain low insulin level during the most of the day and at night.
****************************************************************** IT HAS NOTHING TO DO WITH VEGETABLES OR WITH PLANT VERSUS ANIMAL DIET!!! *****************************************************************
Do you know of any data linking fasting insulin level with any type of disease?I'm sure the connection has been explored hundreds if not thousands of time.....you don't hear doctors or the medical profession talking about it very much so I wonder if there is any significant amount of science to back it up.
If I find any science on this I'm going to ask for a fasting insulin test next lab work.
At he same time my insulin level was 2.0 my blood pressure was spiking to 180 which is contrary to this study....
Fasting Insulin Level Is Positively Associated With Incidence of Hypertension Among American Young Adults: A 20-year follow-up study.Xun P , Liu K , Cao W , Sidney S , Williams OD , He K .SourceCorresponding author: Ka He, firstname.lastname@example.org. AbstractOBJECTIVE Although hyperinsulinemia, a surrogate of insulin resistance, may play a role in the pathogenesis of hypertension (HTN), the longitudinal association between fasting insulin level and HTN development is still controversial. We examined the relation between fasting insulin and incidence of HTN in a large prospective cohort. RESEARCH DESIGN AND METHODS A prospective cohort of 3,413 Americans, aged 18-30 years, without HTN in 1985 (baseline) were enrolled. Six follow-ups were conducted in 1987, 1990, 1992, 1995, 2000, and 2005. Fasting insulin and glucose levels were assessed by a radioimmunoassay and hexokinase method, respectively. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% CIs of incident HTN (defined as the initiation of antihypertensive medication, systolic blood pressure "265140 mmHg, or diastolic blood pressure "26590 mmHg). RESULTS During the 20-year follow-up, 796 incident cases were identified. After adjustment for potential confounders, participants in the highest quartile of insulin levels had a significantly higher incidence of HTN (HR 1.85 [95% CI 1.42-2.40>; P(trend) < 0.001) compared with those in the lowest quartile. The positive association persisted in each sex/ethnicity/weight status subgroup. A similar dose-response relation was observed when insulin-to-glucose ratio or homeostatic model assessment of insulin resistance was used as exposure. CONCLUSIONS Fasting serum insulin levels or hyperinsulinemia in young adulthood was positively associated with incidence of HTN later in life for both men and women, African Americans and Caucasians, and those with normal weight and overweight. Our findings suggested that fasting insulin ascertainment may help clinicians identify those at high risk of HTN. PMID: 22511258 [PubMed - in process> P
Clin Cardiol. 2006 Jan;29(1):25-30.Relationship between true fasting plasma insulin level and angiographic characteristics of coronary atherosclerosis.Jia EZ , Yang ZJ , Yuan B , Zang XL , Wang RH , Zhu TB , Wang LS , Chen BO , Cao KJ , Huang J , Ma WZ .SourceDepartment of Cardiovascular Medicine, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China. email@example.com AbstractBACKGROUND: Reports about the relationships between specific insulin concentration and coronary heart disease risk are controversial. HYPOTHESIS: The objective of this study was to examine the association between insulin level and the severity of coronary atherosclerosis. METHODS: The study population consisted of 507 consecutive patients (376 men and 131 women) who underwent coronary angiography for suspected or known coronary atherosclerosis. The patients' habits of smoking and drinking were investigated, and anthropometric measurements including body mass index, systolic and diastolic blood pressures, as well as plasma measurements including lipids and blood glucose were taken. The true insulin level was measured using a highly sensitive two-site sandwich ELISA. The severity of coronary atherosclerosis was defined by the Gensini score system. The statistical methods including Kruskal-Wallis test, chi-square analysis, Spearman correlation analysis, and multivariate stepwise linear regression analysis were employed to explore the relationship between specific insulin level and coronary atherosclerosis. RESULTS: When the Gensini score was examined as a categorical variable classified by tertile values, subjects with a high Gensini score had significantly higher values of fasting plasma specific insulin level (p = 0.022). The Spearman correlation analysis suggest that the Gensini score correlated significantly with true insulin (mIU/l) (r = 0.095, p = 0.033). However, the results from the multivariate stepwise linear regression analysis show that the association between specific insulin level and severity of coronary atherosclerosis lost its significance. CONCLUSIONS: The level of plasma fasting specific insulin was associated significantly with the severity of coronary atherosclerosis, as measured by Gensini score, but hyperinsulinemia showed no association with the severity of coronary atherosclerosis in multivariate analyses. PMID: 16477774 [PubMed - indexed for MEDLINE> Publication Types, MeSH Terms, Substances Publication Types
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