I watched a podcast about a month ago where Dr Baraki was talking about statins and LDL and how your LDL correlates with your CVD risk, and if I remember correctly, not just now but downstream. This makes sense in many ways, but I’m curious, in literature have t here been any studies assessing cardiovascular disease risk in two groups in the following way:
group one, high HDL, high tri, high LDL
group two, high HDL, low tri, high LDL
Did group two also show a higher CVD risk, both in their age group and lower life expectancy due to CVD risk downstream?
It looks like the only variable that changes in those two scenarios is blood triglyceride levels. Since TGs are their own risk factor for cardiovascular disease, having higher levels confers greater risk compared with lower levels, when all else is equal.
It sounds like you may have listened to our podcast on the topic, and our friends at Sigma have also created more detailed information on this as well:
HCLowFat diet…your LDL goes up but your triglycerides go down since the start of the diet…this is typical from what I’ve read…does your CVD rate go up, or not?
what would the rates of CVD generally be with high hdl, low tri, high ldl? From what I understood once you control for low tri, the high LDL is still the best predictor for CVD?
This is not necessarily what I would expect from a high-carb, low-fat diet, although there are a variety of possible outcomes based on the actual foods included (i.e., what types of carbohydrates, what types of fats, amount of saturated vs. polyunsaturated fats, amount of fiber intake can all change the effects).
You can’t really provide “general rates of CVD” with this little information, unfortunately. With that pattern I would expect less CVD compared to the more classic “atherogenic phenotype” (low HDL-C, high TG, high LDL-C), but cumulative lifelong exposure to apolipoprotein B in the blood is the primary driver of risk, as you will learn from reading those articles I linked above.
FYI Doc this is a long post and more of my thoughts written down. You have no obligation to answer this . I appreciate your pointing me into the right direction with the sigma articles
Got to read it Dr. Baraki. Really cool stuff I shared with a number of physicians in my family, some of whom did not know as much about cholesterol and as it relates more advanced blood lipid paneling and were happy to learn. Share with emergency medicine physician, neurosurgeon, pathologist, and cardiologist… The best resource for this among them was the cardiologist.
metabolic syndrome - even low sat fat, you’re still at risk of incrased blood lipids at a higher BMI. For instance many south Asians display metabolic syndrome, ‘skinny fat’ why is this? Is there any research of LDL as an inflammatory marker, ie repairing the ECL?
how are most studies controling for individual metabolic syndrome, high SF:PFA intake, just that they are in a controlled enviromnment? Not all studies held this constraint
in the referrenced sigma nutrition articles (metanalyses in diet cvd for instance). Or is the implication that these reductions were consistent across reducing SFA, ie reduce SFA by one unit reduces, CVD CHD by one unit, ie linerally- for example - for entire populations?
3. does heavy lifting when overweight contribute to atherosclerosis in overweight and obese individuals, and how does it protect normal eight people against atherosclerosis (how is the ECL lining not more damaged with the high blood pressure of weightlifting)? #mub
4. Lets say we are much older…70 years old. Plaque rupturing becomes a real concern. How do you adjust your weight lifting? Even if you lifted lighter weights but took the sets close enough to failure, you could likely achieve similar changes in blood pressure to heavier loads.
Any theory on which might be better for that age group if you guys have worked with older clients?
5. why are doctors perscribing statins in their 70s instead of 20s and 30s? The majority of cumulative damage has been done, no?
Implications for stopping statins once you start them in your 30s 40s, provided you reach your goal of weight loss, blood lipid, etc?
6) “However, while the Mensink et al. meta-analysis based their analysis around the TC:HDL ratio as a more sensitive predictor of risk, more recent analysis, in particular from the Emerging Risk Factors Collaboration have found that the TC:HDL ratio does not offer any superior marker of CVD/CHD risk prediction.”
What are the general PCP reccomendations from this then? Again, just keep LDL low?
Random thought interjection: Beveridge et al., in a 1955 metabolic ward study in the diet on lipids also has N=5, I’m not sure much statistically signicant could be surmised from this.
7) Familial hypo, south Asian, would you recommend Apob. Even a cardiologist I saw seemed dismissive of this for both me and my father? I wish I could track this for my father pre and post his open heart surgery.
8) any longitudinal studies, 30years+ on statin effects?
9) hdl not spoken a lot about. my sister has a generalized hdl of 68 on reports, wouldn’t a higher C mean its carrying more cholesterol picked up from the blood to be metabolized?
her bmi and waist are excellent <15%bf her ldl is a little high at 118. I haven’t read anything bad in literature about hdl, but the pathologist in the group did say there is evidence of very high HDL not being heart protective?
Glad you found the articles helpful. I will say that many of your questions are far too broad to answer easily in this forum. Several of them can also be addressed by searching for research on the topic.
metabolic syndrome - even low sat fat, you’re still at risk of incrased blood lipids at a higher BMI. For instance many south Asians display metabolic syndrome, ‘skinny fat’ why is this? Is there any research of LDL as an inflammatory marker, ie repairing the ECL?
There is ample discussion of this in the literature. For example, a quick search turned up:
how are most studies controling for individual metabolic syndrome, high SF:PFA intake, just that they are in a controlled enviromnment? Not all studies held this constraint in the referrenced sigma nutrition articles (metanalyses in diet cvd for instance). Or is the implication that these reductions were consistent across reducing SFA, ie reduce SFA by one unit reduces, CVD CHD by one unit, ie linerally- for example - for entire populations?
You’ll need to read individual studies to determine this for each one, regarding things like inclusion/exclusion criteria.
does heavy lifting when overweight contribute to atherosclerosis in overweight and obese individuals, and how does it protect normal eight people against atherosclerosis (how is the ECL lining not more damaged with the high blood pressure of weightlifting)?
No it does not contribute to atherosclerosis. Protective effects of resistance exercise on cardiovascular function are too numerous to list here.
Chronic hypertension does indeed have harmful effects on vasculature, but the fleeting, transient fluctuations in blood pressure during resistance exercise induce adaptive responses in the vasculature that improve reactivity/capacitance — this is part of how chronic resistance exercise lowers resting blood pressure.
Lets say we are much older…70 years old. Plaque rupturing becomes a real concern. How do you adjust your weight lifting? Even if you lifted lighter weights but took the sets close enough to failure, you could likely achieve similar changes in blood pressure to heavier loads. Any theory on which might be better for that age group if you guys have worked with older clients?
Again, the transient fluctuations in blood pressure during appropriately-dosed resistance exercise do not have harmful effects on the vasculature. I do not modify resistance training on the basis of age alone.
There are numerous papers out there on the mechanisms of plaque formation, vulnerability, and rupture that you can find with a quick search.
why are doctors perscribing statins in their 70s instead of 20s and 30s? The majority of cumulative damage has been done, no?
Yes, but what would you propose they do for someone who is at high cardiovascular risk and has not been treated to date, for whatever reason?
Implications for stopping statins once you start them in your 30s 40s, provided you reach your goal of weight loss, blood lipid, etc?
If achieving these goals results in sufficient low cardiovascular risk estimates, then from a primary prevention standpoint it would be reasonable to discontinue statin therapy. However, for individuals at higher risk we have evidence that discontinuation results in higher event rates.
“However, while the Mensink et al. meta-analysis based their analysis around the TC:HDL ratio as a more sensitive predictor of risk, more recent analysis, in particular from the Emerging Risk Factors Collaboration have found that the TC:HDL ratio does not offer any superior marker of CVD/CHD risk prediction.” What are the general PCP reccomendations from this then? Again, just keep LDL low?
We do not use ratios, and do not recommend the use of ratios for clinical decision making. We aim to keep non-HDL-C (or ApoB, if measured) low.
Random thought interjection: Beveridge et al., in a 1955 metabolic ward study in the diet on lipids also has N=5, I’m not sure much statistically signicant could be surmised from this.
Statistical significance does not depend solely on the sample size, but also on the size of the effect. Regardless, even if you were correct, there are literally hundreds of other controlled feeding trials in this area that point in the same direction.
Familial hypo, south Asian, would you recommend Apob. Even a cardiologist I saw seemed dismissive of this for both me and my father? I wish I could track this for my father pre and post his open heart surgery.
I’m not sure what the question is here.
any longitudinal studies, 30years+ on statin effects?
Statins are among the most studied drugs in existence, and there are long-term data sets, but these drugs were discovered and produced in the late 1980s/early 1990s.
hdl not spoken a lot about. my sister has a generalized hdl of 68 on reports, wouldn’t a higher C mean its carrying more cholesterol picked up from the blood to be metabolized?
Not necessarily. While higher HDL-C levels are associated with better outcomes, interventions to directly raise HDL-C have not shown cardiovascular benefit.
Doc how about Dave Feldman who cites te Framingham Offspring study is still the best so far and it appears to showcase LDL+:arrow_up:HDL+:arrow_down:Trigs=Reduced CVD risk ?
This seems to contradict at times that LDL has a linear relationship with CVD, or are BOTH relationships valid but the GREATEST cvd reduction in is just lowering your LDL?
LDL+:arrow_up:HDL+:arrow_down:Trigs=Reduced CVD risk ?