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Gabriel cousens talk
Posted by: fresh ()
Date: March 02, 2018 06:56AM

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Re: Gabriel cousens talk
Posted by: John Rose ()
Date: March 02, 2018 01:58PM

Thanks fresh, lots of good info in there that I've heard before about Low Fat and Low Cholesterol, however, Cousens' math does NOT add up for the Macronutrients - see below.

13:19 MM
Here is the research I want you to see. This is the research I’ve done. This is not theory. This is the research I’ve done is that an adequate Live Food Diet 25-45% Fat; 25-45% Complex Green Carbohydrates - I’m talking about Vegetables, Fruit, Leafy Greens, Sprouts - that’s what I’m talking about, ok, and 10-20% Protein depending on your Constitution. So that’s the overall Macronutrient Ratio I’m focusing on. 13:52 MM

Optimal Macronutrient Ratio [Slide]

25-45% Fat

10-20% Protein

25-45% Carbohydrate

JR Comment:

These numbers do NOT add up.

For example, if we choose the low ends for Fat and Protein, we’ll need 65% Carbohydrate and if we if we choose the high ends for Fat and Protein, we’ll need 35% Carbohydrate.

So 25% Carbohydrate is too low if we choose the high ends for Fat and Protein and 45% Carbohydrate is too low if we choose the low ends for Fat and Protein.

In other words, Carbohydrates should be 35-65% Carbohydrate if we are going to use Cousens’ Fat and Protein %s because ...

25 + 10 + 45 = 80% and
45 + 20 + 25 = 90%,

whereas, if we use 35-65% Carbohydrate, we get

25 + 10 + 65 = 100% and
45 + 20 + 35 = 100%.

So if we’re going to use Cousens’ Fat and Protein %s, his Optimal Macronutrient Ratio should be…

25-45% Fat

10-20% Protein

35-65% Carbohydrate

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Re: Gabriel cousens talk
Posted by: fresh ()
Date: March 02, 2018 02:07PM

Good points JR

I find all his claims suspect anyway.


Spiritual oriented people allow their unscientific ideas to bleed into what should be science.

And he says he did 26 pullups til he started e3live then he did 32. Yeah ok, whatever...
That's more doable than the numbers in the hundreds that were posted here a while back but still I wait for the video.

And we need the specific studies and context he claims support low cholesterol being a negative factor

Edited 2 time(s). Last edit at 03/02/2018 02:11PM by fresh.

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Re: Gabriel cousens talk
Posted by: John Rose ()
Date: March 02, 2018 04:18PM

Here's a snippet from my File Preview on Cholesterol about the Norway Study, so if you live in Norway, you might want to heed this Study.

Is the use of cholesterol in mortality risk algorithms in clinical guidelines valid? Ten years prospective data from the Norwegian HUNT 2 study

• Abstract
• Rationale, aims and objectives
• Many clinical guidelines for cardiovascular disease (CVD) prevention contain risk estimation charts/calculators. These have shown a tendency to overestimate risk, which indicates that there might be theoretical flaws in the algorithms. Total cholesterol is a frequently used variable in the risk estimates. Some studies indicate that the predictive properties of cholesterol might not be as straightforward as widely assumed. Our aim was to document the strength and validity of total cholesterol as a risk factor for mortality in a well-defined, general Norwegian population without known CVD at baseline.
• Methods
• We assessed the association of total serum cholesterol with total mortality, as well as mortality from CVD and ischaemic heart disease (IHD), using Cox proportional hazard models. The study population comprises 52 087 Norwegians, aged 20–74, who participated in the Nord-Trøndelag Health Study (HUNT 2, 1995–1997) and were followed-up on cause-specific mortality for 10 years (510 297 person-years in total).
• Results
• Among women, cholesterol had an inverse association with all-cause mortality [hazard ratio (HR): 0.94; 95% confidence interval (CI): 0.89–0.99 per 1.0 mmol L?1 increase] as well as CVD mortality (HR: 0.97; 95% CI: 0.88–1.07). The association with IHD mortality (HR: 1.07; 95% CI: 0.92–1.24) was not linear but seemed to follow a ‘U-shaped’ curve, with the highest mortality <5.0 and ?7.0 mmol L?1. Among men, the association of cholesterol with mortality from CVD (HR: 1.06; 95% CI: 0.98–1.15) and in total (HR: 0.98; 95% CI: 0.93–1.03) followed a ‘U-shaped’ pattern.
• Conclusion
• Our study provides an updated epidemiological indication of possible errors in the CVD risk algorithms of many clinical guidelines. If our findings are generalizable, clinical and public health recommendations regarding the 'dangers' of cholesterol should be revised. This is especially true for women, for whom moderately elevated cholesterol (by current standards) may prove to be not only harmless but even beneficial.
• Introduction

• The incidence, prevalence and mortality from CVD have decreased substantially throughout the Western world in recent decades [79,80]. There are also significant time trend changes regarding various risk factors for CVD [81–83]. Changes have occurred, both regarding risk factors frequently included in combined risk estimates [83–85] and for factors such as societal structure [86,87], pollution [88], television viewing [89] and dietary habits [90,91]. These on-going changes are likely to alter the predictive value of risk algorithms based on observational data collected years or even decades ago (retrospective risk bias). As cholesterol has become an essential part of lay-people's basic understanding of their health, and the prevalence of slightly ‘elevated’ cholesterol levels is so high, we believe that it is important to re-examine old assumptions regarding cholesterol as a risk factor.
• The aim of the present study was to document the strength and validity of total serum cholesterol as a risk factor for mortality, as defined by current CVD prevention guidelines. For this purpose, we used data from a well-defined, general Norwegian population without known CVD at baseline. We focused on deaths from cardiovascular disease, IHD and death from all causes (total mortality) within a follow-up period of 10 years.
• Methods
• Study population
• All adults, aged 20 years or older and living in Nord-Trøndelag County in Norway in 1995–1997, were invited to participate in the second wave of the Nord-Trøndelag Health Study (HUNT 2). Overall, 74% of women (34 786) and 65% of men (30 575) chose to participate. The HUNT 2 population is ethnically homogeneous (dominated by individuals of Nordic origin) and has been considered fairly representative of the total Norwegian population with respect to demography, socio-economic factors, morbidity and mortality, including mortality from CVD [92]. The HUNT 2 study has been described in detail elsewhere (see []) [92].
• For the purpose of the present analysis, the following HUNT 2 participants were excluded: 6780 individuals aged 75 years or more at baseline (2815 men and 3965 women); 3430 individuals (2207 men and 1223 women) with established CVD at baseline (self-reported myocardial infarction, stroke or angina pectoris); and 3064 persons with missing data on one or more of the following variables: serum cholesterol, systolic blood pressure and smoking status. Our calculations are thereby based on information from 52 087 individuals (24 235 men and 27 852 women) aged 20–74 years and free from known CVD at baseline.
• Study variables
• In the HUNT 2 survey, total serum cholesterol was measured by an enzymatic colorimetric cholesterol esterase method [92]. The blood pressure of persons in a seated position was measured by a specially trained personnel using Dinamap 845XT, based on oscillometry. The cuff size was adjusted after measuring the arm circumference, and blood pressure was recorded as the mean values of the second and third measurements performed consecutively at the same visit. Smoking was defined as daily smoking of cigarettes, cigars or a pipe.
• Follow-up
• The personal identity number of Norwegian citizens enabled linking of HUNT 2 participant data to the Cause of Death Registry at Statistics Norway (information on []). For the present analysis, each participant contributed person–time from the date of clinical examination (August 1995–June 1997) until 10 years of follow-up had been achieved (until August 2005–June 2007, depending on participation dates) or until the date of death if this occurred in the follow-up period, making the oldest participants of the study 84 years of age at the end of the follow-up. The follow-up time came to a total of 510 297 person-years. Death from CVD was defined by the International Classification of Disease code for the primary diagnosis of death (ICD-9: 390-459; ICD-10: I 00-I 99) as well as death from IHD (ICD-9: 410-414; ICD-10: I 20-I 25).
• Statistical analysis
• Ethics statement

• Results
• Figure 1 shows CVD mortality for the HUNT 2 population during the 10-year follow-up period (mortality rates per 1000 person-years), according to each level of the risk factors found in the international SCORE system. This model showed a general trend towards increased mortality for an increase in any of the included risk factors, except for cholesterol, where no such association was observed. The results were similar regarding all-cause mortality and IHD mortality (data not shown).
• Table 1 shows the sex-specific associations of different levels of serum cholesterol with mortality, both total mortality and CVD and IHD mortality. Among women, serum cholesterol had an inverse association with all-cause mortality as well as CVD mortality (although not reaching statistical significance) (Table 1). The association with IHD mortality appeared to follow a U-shaped curve. Test for quadratic trend did not support the existence of a U-shaped curve (P = 0.16).

• Smoking, on the other hand, was strongly associated with increased mortality in all mortality categories among both sexes (Table 3). Among women, the association was somewhat stronger for those with cholesterol below 5.5 mmol L?1 [5.5 = 213].

• Discussion
• In this validation study of current guidelines for CVD prevention, which is based on new epidemiological data from a large and representative Norwegian population, we found total cholesterol to be an overestimated risk factor.
• Regarding the association between total cholesterol and mortality, our results generally indicated U-shaped or inverse linear curves for total and CVD mortality. Only the association with IHD among men could be interpreted as suggesting a positive, linear trend.
• Our results contradict the guidelines' well-established demarcation line (5 mmol L?1) between ‘good’ and ‘too high’ levels of cholesterol. They also contradict the popularized idea of a positive, linear relationship between cholesterol and fatal disease. Guideline-based advice regarding CVD prevention may thus be outdated and misleading, particularly regarding many women who have cholesterol levels in the range of 5–7 mmol L?1 [5-7 = 193-271] and are currently encouraged to take better care of their health.

• To address the question of whether the U-shaped association was age-dependent in the HUNT population, we performed an age-stratified Cox-regression analysis post-hoc. The results indicated a U-shaped association of cholesterol with CVD mortality among men aged 40–74, and an inverse association among women aged 60–74. Because of limited statistical power, we refrain from emphasizing these results. Seen in the light of previous studies [37,55,58,61,64–66,73–77], it is possible that a U-shaped association is primarily a phenomenon related to people aged 60 years and older.

• Conclusions
• Based on epidemiological analysis of updated and comprehensive population data, we found that the underlying assumptions regarding cholesterol in clinical guidelines for CVD prevention might be flawed: cholesterol emerged as an overestimated risk factor in our study, indicating that guideline information might be misleading, particularly for women with ‘moderately elevated’ cholesterol levels in the range of 5–7 mmol L?1. Our findings are in good accord with some previous studies. A potential explanation of the lack of accord between clinical guidelines and recent population data, including ours, is time trend changes for CVD/IHD and underlying causal (risk) factors.
• ‘Know your numbers’ (a concept pertaining to medical risk factor levels, including cholesterol) is currently considered part of responsible citizenship, as well as an essential element of preventive medical care. Many individuals who could otherwise call themselves healthy struggle conscientiously to push their cholesterol under the presumed ‘danger’ limit (i.e. the recommended cut-off point of 5 mmol L?1), coached by health personnel, personal trainers and caring family members. Massive commercial interests are linked to drugs and other remedies marketed for this purpose. It is therefore of immediate and wide interest to find out whether our results are generalizable to other populations.
• Funding
• This work was supported by the Research Unit of General Practice, Department of Public Health and General Practice, Norwegian University of Science and Technology (NTNU), Trondheim, Norway; the Norwegian Medical Association's Funds for Research in General Practice; and the Research Fund of the Icelandic College of Family Physicians.
• Acknowledgments

• Conflicts of interest
• The authors declare no conflicts of interest.
• References


Edited 2 time(s). Last edit at 03/02/2018 04:19PM by John Rose.

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Re: Gabriel cousens talk
Posted by: Tai ()
Date: March 03, 2018 12:37AM

One of his points is that he wants his clients to have a cholesterol above 159. So what I would like to know is what percentage of coconut fat his clients are eating to achieve that, if they are.

And it seems weird to be recommending coconut oil, when fresh coconuts are sold everywhere.

is this the study that shows low cholesterol is correlated with higher suicide risk? This is a very small study.

I would assume they have ruled out cancer, which obviously would increase suicidal feelings and also lowers cholesterol.

look at this:

In this prospective sample of depressed patients, an association was not found between severe suicide attempts and low cholesterol levels. This finding is in contrast with a previous analysis of the same data set demonstrating an association between low cholesterol levels and suicide completions (Coryell and Schlesser, in press). The current analysis not only fails to support the initial hypothesized association between low baseline cholesterol levels and subsequent severe suicide attempts, it suggests the contrary, a finding which persists when extended to include all suicide attempts. Exploration of a cholesterol group by age interaction further reveals that the high cholesterol group has more suicide attempts in only those below median age.

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Re: Gabriel cousens talk
Posted by: fresh ()
Date: March 03, 2018 07:22AM

by the way, blue zones eat on average
65% carbs
20% fats
15% protein

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