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Old 15-05-2018, 05:16 PM   #46
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i eat the loti.

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Old 15-05-2018, 05:18 PM   #47
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Yr mum prob has vascular dementia from yr high chol diet. Egg yolks r known to increase bad chol.
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Old 15-05-2018, 05:27 PM   #48
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Yr mum prob has vascular dementia from yr high chol diet. Egg yolks r known to increase bad chol.
You are SO WRONG there !

Just WHEN will you ever get it that the Great Cholesterol Myth
- has been DEBUNKED for years already etc ?????

Go read this https://www.healthline.com/nutrition...should-you-eat


or even this post among my MANY posts on cholesterol
Eggs & Cholesterol
https://forums.hardwarezone.com.sg/1...77-post21.html
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Old 15-05-2018, 05:41 PM   #49
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You are SO WRONG there !

Just WHEN will you ever get it that the Great Cholesterol Myth
- has been DEBUNKED for years already etc ?????

Go read this https://www.healthline.com/nutrition...should-you-eat


or even this post among my MANY posts on cholesterol
Eggs & Cholesterol
https://forums.hardwarezone.com.sg/1...77-post21.html
Sorry, I prefer to be taught by real life certified medical teachers and Drs than dubious sources.
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Old 15-05-2018, 05:44 PM   #50
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siao lang spotted
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Old 15-05-2018, 05:58 PM   #51
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Sorry, I prefer to be taught by real life certified medical teachers and Drs than dubious sources.
Be taught then .....

https://blog.virtahealth.com/blood-l...etogenic-diet/

Blood Lipid Changes With A Well-Formulated Ketogenic Diet In Context: Understanding the Total Risk ‘Forest’ Rather than Focusing on the ‘LDL Tree’

Rich Wood, PhD Amy McKenzie, PhD Jeff Volek, PhD, RD Stephen Phinney, MD, PhD
on May 2, 2018

Introduction

For the last 5 decades, most medical and nutrition scientists have focused on low density lipoprotein (LDL) cholesterol as a primary cause of coronary heart disease. Characterized as ‘bad cholesterol’, literally thousands of studies have been done using drugs or diet to reduce LDL cholesterol and thereby hoping to reduce heart attacks and mortality. While cholesterol lowering therapy has become the standard of care for some individuals with well-defined heart disease risk, this focus on cholesterol in general—and LDL cholesterol in particular—remains very controversial.

Part of this controversy stems from our tendency as scientists to reduce a problem to its simplest component(s). Unfortunately the standard measure of blood LDL cholesterol is easy but inaccurate (Volek Phinney 2011), and even when the various components of the blood LDL are accurately measured (Reaven 1993) they represent only a fraction of the lipid and other biomarkers of heart disease risk. In other words, in the interest of ‘keeping it simple’, we have wrongly ignored the rest of the ‘forest’ of other risk factors while focusing on the LDL cholesterol ‘tree’.

A turning point in understanding the limitations of LDL and heart disease came with the publication of the Lyon Diet Heart Study (de Lorgeril 1994, 1999).
This randomized trial pitted a standard low fat diet against a Mediterranean diet for people with a prior heart attack. The study was halted after 2.7 years because there was a dramatic reduction in repeat heart attack incidence and overall mortality in the Mediterranean diet group. But to everyone’s astonishment, there was no difference in LDL cholesterol changes between the Mediterranean and low fat diet groups. At least for this diet study, the standard calculated LDL value did not seem to matter that much. Nor did most of the other standard biomarkers of that era that they measured, indicating that some very important drivers of coronary disease risk were going unmeasured. In the intervening 20 years, however, the range of factors linked to heart attack risk has expanded greatly – i.e., the forest has gotten a lot bigger.

In our recently published 1-year results from the IUH/Virta diabetes reversal study, we reported a small but significant rise in the average blood LDL cholesterol level in our patients on a well-formulated ketogenic diet (Hallberg, 2018). At the same time, however, we noted major reductions in a number of coronary disease risk factors including weight, blood pressure, and of course HbA1c. But now we have published a much more extensive review of these risk factor changes for this group of about 200 patients after a year of Virta Treatment (Bhanpuri 2018). As a snap-shot of this ‘tree view’ versus a ‘forest view’, here are two contrasting figures that demonstrate just how complex this picture is, but also the pattern of how these other risk factors change independent of the variable changes in LDL.


... etc ...


What Blood Lipids Actually Do

When we think of various tests as risk factors, we sometime tend to forget what those substances actually do in the body and why their levels change (or not) when we change our diet. For example, we have known for a long time that blood levels of both cholesterol and saturated fat tend to be independent of how much of these nutrients we eat. (Volek Phinney, The Sad Saga of Saturated Fat; Volek Phinney, You Are Not What You Eat). For other essential nutrients like omega-3 fats, blood and tissue levels tend to be quite responsive to dietary intakes.

But a completely different set of factors come into play when we eat less energy than we burn, which forces the body to dip into its energy stores and thus mobilize body fat. Similarly, when we restrict dietary carbohydrates, either body fat or dietary fat has to become the body’s principle source of energy. This is most profound in the keto-adapted state, where circulating lipids and blood ketones (made from fat in the liver) together provide 75-85% of the body’s energy. In other words, eating more fat requires that more of it pass through the bloodstream. Lipoproteins play a critical role in the transport of lipid in the bloodstream, so changes in delivery needs in turn will impact lipoprotein lab results.

In reality, the changes in how the body processes, transports, and uses fat for energy after becoming keto-adapted are very complex. In response to the state of nutritional ketosis, humans can more than double their rates of fat oxidation (i.e., use for fuel) at rest and during exercise (Phinney 1983, Volek Phinney 2012, Volek 2016). So when you combine a doubling of fat intake with a doubling of fat use, clearly a lot more fat has to pass through the bloodstream. And the mysteries here are how and why this can be safely accomplished, and how these dramatic changes in fat transport are reflected in a standard fasting blood lipid panel.

We have spent a few decades studying how the body adapts to a well-formulated ketogenic diet, and have come to recognize a pretty consistent pattern for the changes in most blood lipids, but a quite inconsistent pattern for the calculated LDL cholesterol level in particular. The consistent changes are:

-a dramatic reduction in serum triglycerides

-a rise in HDL cholesterol

-and the same or lower levels of saturated fats in serum triglycerides


As noted above, the one inconsistent variable in this otherwise predictable pattern of change is the calculated serum LDL cholesterol level. For some people, following a ketogenic diet makes their LDL cholesterol go down and for some it does not change. But for a fair number of people the calculated LDL cholesterol value rises, in some cases quite a lot. Thus the key question from this topic is: How important is the calculated LDL cholesterol relative to the other risk factors that have been recently characterized?

Why LDL Cholesterol is Not a Single Number

There are two important limitations of the commonly reported serum LDL cholesterol level. First, the usual test procedure does not actually measure LDL – it reports a calculated value based upon measurements of serum total and HDL cholesterol and triglycerides, along with a number of assumptions. And in particular, when the triglyceride value undergoes a big change, it can skew the calculated LDL value considerably (Volek Phinney 2011). Second, the circulating lipoprotein particles classed as LDL are actually quite diverse in size, and it is now recognized that the smaller, more dense particles (which carry proportionately less triglyceride) are the sub-fraction that is associated with vascular damage and heart disease (Austin 1988, Berneis 2002).

As noted in our recent study data, all but one of the biomarkers of cardiovascular risk that we measured moved in a beneficial direction, and for most of these the changes were statistically significant. Only the calculated LDL cholesterol value went in the ‘wrong direction’. But in this case, it appears that this was due to a shift to a greater proportion of the larger particles because the total particle number did not change, the average particle size increased, while the small dense particle number was significantly decreased.

Inflammation as an Independent Risk Factor for Coronary Vascular Disease

The idea that there are other important CVD risk factors beside cholesterol and its distribution among lipoproteins is not new. Starting over three decades ago, a number of mainstream investigators have noted that the total white blood cell count (Yarnell 1985, Kannel, 1992) and then c-reactive protein (Ridker 1996) levels appear to predict coronary disease and mortality independent of cholesterol.

The key question as to whether this was a mere association or causal has been addressed by two major studies. The JUPITER study assessed the response of patients with high CRP but non-elevated LDL cholesterol levels to the anti-inflammatory effects of a statin drug (Ridker 2008). Coronary events were significantly reduced within 2 years, but the effects of the statin on inflammation compared to further reductions in LDL cholesterol could not be definitively separated. This question was resolved with the recent CANTOS Trial (Ridker 2017), in which a mono-clonal antibody against IL-1 beta reduced coronary risk by 15% without any effect on LDL cholesterol levels.

Unfortunately a side effect of of the antibody used in this study (an increase ion fatal infections) cancelled out the coronary disease risk reduction, so the CANTOS Trial answered an important question but did not offer an therapeutic solution. However this does offer an interesting insight into the mystery of why the Lyon Diet Heart Study reduced coronary disease risk AND mortality. In that study, blood anti-oxidant levels increased and granulocytes (aka white blood cells) decreased, suggesting that a dietary anti-inflammatory intervention can have potent benefits absent the dangerous side-effects of anti-inflammatory drugs.

Seen from this perspective, the statistically robust anti-inflammatory effects observed in our current study highlight a demonstrably important portion of the coronary disease ‘risk forest’ that is independent of cholesterol.

Blood Saturated Fats and CVD Risk

The levels of saturated fats in various blood lipid fractions—and particularly the 16-carbon saturated fat called palmitate—have long been known to be correlated with risk for heart disease, type 2 diabetes, and mortality (Wang 2003). We have previously posted a detailed review of this topic in our blog The Sad Saga of Saturated Fat. The key fact to keep in mind is that while a primary source of saturated fat in the blood is de novo lipogenesis (i.e., the production of fat from excess dietary carbohydrate) (Aarsland 2003), there is little if any relationship between dietary saturated fat intake and blood saturated fat content. And most importantly, because the keto-adapted state doubles the body’s ability to burn saturated fat for fuel while at the same time shutting down de novo lipogenesis, blood levels of saturated fats are reduced independent of dietary saturated fat intake (Forsythe 2008 & 2010, Volk 2014). Thus we have another disconnect between dogma and data: a risk factor that goes down with a well-formulated ketogenic diet despite the ‘diet-heart disease hypothesis’ which tries to link dietary saturated fat to blood cholesterol levels.

Getting Beyond Single Biomarkers of Cardiovascular Risk

Given the host of biomarkers reflecting a wide range of processes that contribute to atherosclerosis and coronary artery disease risk, the recognition that we need a multifactorial equation that encompasses this heterogeneous process rather than striving for a single reductionist approach is finally gaining traction (Yeboah 2016). Based upon published 2013 guidelines, the American College of Cardiology now offers a 10-year heart disease risk predictor that includes the following inputs:

age
sex
race
total cholesterol
HDL cholesterol
LDL cholesterol
systolic blood pressure
diastolic blood pressure
diabetes
smoking
medication use
statin
hypertension
aspirin

Based upon this equation, the 10-year atherosclerotic cardiovascular disease (ASCVD) risk score in our recent study decreased -11.9% (P = 510-5). This is a large beneficial effect experienced by the participants in our study despite the observed changes in calculated LDL values. And this equation does not take into account improvements in inflammation and saturated fats that would reduce this risk prediction even further.

Summary

Biomarkers of cardiovascular disease risk represent our scientific attempt to find a crystal ball that predicts future disease and guides rational therapeutic intervention. In a case where so many different factors are associated with coronary risk, we need to avoid the reductionist temptation to focus on a single tree over the contribution of the entire forest.

Ideally, in the future we will have results on CVD and mortality risk from a large randomized controlled trial pitting a well-formulated ketogenic diet against the best that usual care can offer. In the interim, we have demonstrated that a continuous care treatment including nutritional ketosis in patients with type 2 diabetes improved most biomarkers of CVD risk after one year. The increase in LDL-cholesterol appeared limited to the large LDL sub-fraction; whereas LDL particle size increased, total LDL-P and ApoB were unchanged, and inflammation and blood pressure decreased.

Last edited by kaypohchee; 15-05-2018 at 06:01 PM..
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Old 15-05-2018, 06:02 PM   #52
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This is the LOWEST in the Disagreement Hierarchy - Name Calling

Aiyoh get some class bah ..... want to disagree - disagree with some style


Last edited by kaypohchee; 15-05-2018 at 06:06 PM..
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Old 15-05-2018, 06:08 PM   #53
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I am not comfortable with online medical google resources. I trust hard copy medical journals more. Even in our CME talks, we r told google is not our best friend.
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Old 15-05-2018, 06:16 PM   #54
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We individually risk stratify each pt. One may need LDL less than 100 while another less than 160. That is what Drs r for.
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Old 15-05-2018, 06:17 PM   #55
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I am not comfortable with online medical google resources. I trust hard copy medical journals more. Even in our CME talks, we r told google is not our best friend.
Just sent you a PM re trusted medical & scientific journals & studies online.
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Old 15-05-2018, 06:46 PM   #56
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OMG - No BLIND bowing to so-called health authorities such as WHO for me - they were SO Wrong demonising coconut oil - we must be able to think & rationalise independently etc

https://twitter.com/gillespi/status/996219761401806848

David Gillespie
‏@gillespi
Follow Follow @gillespi
More David Gillespie Retweeted Alexandra Jones
Unfortunately this 'initiative' is not remotely based on science. They want trans fats (made from seed oils) replaced with seed oils. Seed Oils not made into trans fats are even more deadly than the ones that are. The WHO initiative will massively accelerate chronic disease


Alexandra Jones
@alikjones
This is an important initiative. There is no place for transfat in the global food supply. Industry must voluntarily remove, or face totally reasonable regulation. https://twitter.com/LinaMahyl/status...761279791108

7:44 PM - 14 May 2018


Joris Snellenburg
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Replying to @gillespi
I fully agree with the notion of avoiding seed oils, but could you elaborate on how (unstable) (polyunsaturated) (rich-in-ω6) seed oils are even more dangerous than trans fat? Because that could help to convince a lay person who is already aware of the danger of trans fat.



David Gillespie
‏@gillespi
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Unstable ω6 significantly increases cell membrane oxidation and (as a consequence) DNA damage. The process is almost identical to how smoking causes cancer but distributed throughout every cell in the body. My book Toxic Oil goes into it in more detail.


Melody PattisonMehta
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I completely agree. These "public health policy" groups can be shockingly clueless. They also fail to distinguish between natural and synthetic/industrial trans fats. Big difference!



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This is just plain wrong, talk about out of the frying pan into the fire!
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Old 15-05-2018, 07:01 PM   #57
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Share please?

Just sent you a PM re trusted medical & scientific journals & studies online.
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eh, seriously, few lines and 100 chars can write what ah?
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Old 15-05-2018, 07:12 PM   #58
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Share please?
Just sent you a PM.
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Old 15-05-2018, 07:21 PM   #59
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All these abbreviations... I had thought LC stood for Low Class
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Old 15-05-2018, 07:35 PM   #60
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kpc, since u practise what u preach, I'm curious what is ur height and weight? i would assume u r on the slim end of the spectrum judging from ur meal photos.
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