5 Steps to prevent Heart Disease

Thursday, December 26, 2013

Kansas City Plaza Club Presentation

Slideshow at Plaza Club

I gave a 20 minute talk on my presentation called Hunger Games.

It was a good group of about 55 men.

I am still trying to hone my talk.
Energy gap is a difficult concept to present especially when adding Energy Expenditure curves.

These three slides are critical concepts that I tried to present:

1-The False Premise
"Dieters can wipe the slate clean, our newer slimmer bodies retain no memory of our larger prior body."
The Weight of the Nation by Hoffman & Salerno pg. 168

2-The Set Point
"The research of Dr. Leibel & Dr. Rosenbaum shows that even after ten years of successfully maintaining a significant weight loss, the body doesn't readjust".

3-Calorie is not a calorie
"Fifty year old 3,500 calorie rule equates weight alteration of one pound to 3,500 cal. deficit/increment.  It ignores the physiological compensation by the body."
Myths, Presumptions, and Facts about Obesity
N Engl J Med 2013; 368:446-454 January 31, 2013

Wednesday, December 25, 2013

Why isn't there a program to prevent the 100,000 sudden coronary deaths?

Essay on my angst over the death of the ATP IV guidelines

Physicians have been waiting for the new NCEP ATP IV guideslines since December 2009.

Last month it was announced there will not be any new guidelines.

In the meantime there are 100,000 sudden deaths a year while no organization addresses the true present ability to prevent these deaths with early diagnosis of plaque by CIMT and CAC and inexpensive and safe treatment with generic statin and over the counter wax matrix niacin called Endur-acin.

As it may have been with James Gandolfini, sudden death is the first sign of the unstable plaque present in the patient in 30 to 50% of the cases.

On July 27, 2013, Kid Kraddick dies during golf game at age 53
 Is this another case of death being the first sign of coronary artery disease?
Will the media ask why there is no program to stop this epidemic of deaths?

Tuesday, December 24, 2013

Update on Exercise Feb 2013

Update on Exercise


Caveat emptor:

“The amount of physical activity necessary to produce health benefits cannot yet be identified with a high degree of precision”
DHHS guidelines 2008

“no randomized trials of physical activity and cancer rates have been conducted”
p. 235 Physical Activity and Health

1-Physical Activity and Health Text
Claude Bouchard, Steven Blair, William Haskell 2nd edition 2012

page 353:
“The International Association for the Study of Obesity concluded that for adults, 45-60 minutes per day is required to prevent the transition to overweight or obesity and that prevention of weight regain in formerly obese individuals requires 60 to 90 minutes of moderate-intensity activity or smaller amounts of vigorous activity (Saris et. al) 2003.
Similar recommendations were made in Dietary Guidelines for Americans 2005 (US Department of Health and Human Services [DHHS} and US Department of Agriculture 2005).”

page 354:
“Global Recommendations on Physical Activity for Health, published by the World Health Organization (WHO) in 2010 shift primary focus away from losing weight and toward first meeting the weekly physical activity target.”  150 minutes per week of moderate-intensity”.

page 82:
“The Heritage Family Study showed that although the average increase VO2 max attributable to an endurance training program was 16%,  some participants did not change at all, and others had an increase of 50%.  The variability in response appears to have a strong genetic link.”

page 395:
“A similar pattern of variation in training responses was observed for:
1- HDL-C
2- Total Cholesterol levels
3- Submaximal exercise heart rate
4- Blood pressure changes
(Bouchard and Rankinen 2001)

page 404:
“endurance training-induced changes in risk factors do not correlate well with changes in cardiorespiratory fitness level.  On the other hand... it is impossible to predict the effects of regular exercise on one risk factor by observing the training response of another risk factor. Thus far we have no indication that there are people who are non-responders across all markers of risk for diseases.  These observations emphasize that even if a person cannot improve cardiorespiratory fitness with regular exercise, it is likely that he will achieve other significant health benefits from a physically active lifestyle.”

page 235:
“The evidence for a role of physical activity in preventing certain cancers comes primarily from epidemiologic studies.  The findings from such studies are supported by plausible biologic mechanisms.”

page 241:
“The data are clearest in support of physical activity or fitness as a means of preventing colon and breast cancers.”

page 227:
“There is now strong epidemiological evidence that regular physical exercise can prevent or delay the onset of type 2 diabetes.”

Monday, December 23, 2013

Niacin update


The Current State of Niacin in Cardiovascular Disease Prevention

A Systematic Review and Meta-Regression

Conclusions  The consensus perspective derived from available clinical data supports that niacin reduces CVD events and, further, that this may occur through a mechanism not reflected by changes in high-density lipoprotein cholesterol concentration.

There was a total of 4,365 subjects allocated to receive niacin intervention and 5,596 subjects allocated to the respective control arms of included trials. The mean duration of follow-up was 2.7 years (SD 1.7 years).  Of the 11 trials included in the primary meta-analysis, 8 were conducted in a double-blind fashion 

Despite clear efficacy demonstrated by multiple clinical endpoint–driven studies, increasing appreciation of the considerable CVD risk that persists despite intensive statin therapy ((4),(5),32) has heightened interest in alternative therapeutic interventions. 

The consensus perspective derived from previously available data had suggested that niacin could be an effective agent in CVD risk prevention ((23),24).
 Although clinical outcome data supporting its benefits largely predate the advent of statins, several recent trials showed niacin to be an effective adjunct to statin therapy with respect to surrogate measures of atherosclerosis progression ((16),(17),(18),(19),(20),21). 

Contrasting evidence provided by results of the AIM-HIGH trial (22) recently called into question the appropriate role of niacin in clinical practice. The present study, taking in aggregate the cumulative body of relevant empirical clinical data, continues to support that niacin is an effective agent to reduce CVD risk.

In the present meta-analysis including a total of 9,959 subjects derived predominantly from secondary prevention trials, allocation to niacin treatment yielded relative odds reductions of 34% (p = 0.007) and 25% (p = 0.02) for the respective endpoints of any CVD event and major CHD event. 

Furthermore, a significant treatment effect remained in analysis limited to those trials evaluating the effect of niacin in combination with statin therapy for the largest composite clinical endpoint of any CVD event. 
Placing these findings in context, the Cholesterol Treatment Trialists' Collaboration recently reported 22% and 27% reductions in comparable clinical endpoints in statin-treated participants compared with a control population in a meta-analysis of 21 trials including 129,526 subjects (5).

While serving to place the recent results of AIM-HIGH in context with the total body of clinical trial evidence, the current analysis challenges prevalent notions surrounding the mechanism underlying the treatment effect of niacin.  

Widely recognized as the most potent currently available modulator of HDL-C, the potential benefit of niacin in mitigating CVD risk is often attributed to its impact on this target. The rationale for this hypothesis is derived from extensive epidemiological data establishing baseline low HDL-C as an independent marker of CVD risk ((33),(34),(35),(36),37).

 It is important to consider, however, that the pharmacological effects of niacin extend well beyond augmentation of HDL-C concentration.

 In the current study, meta-regression failed to demonstrate an association between on-treatment differences in HDL-C concentration and niacin-mediated improvement of outcomes.
 There are several ways in which this finding can be interpreted.
 One possibility is that the clinical efficacy of niacin may still result from its lipid effects, but that these are not captured in the standard lipid measurements reported in clinical trials. For example, niacin reduces lipoprotein (a) and exerts presumably favorable effects on both HDL-C and LDL-C particle size distribution, not reflected by typical lipoprotein analysis nor assessed in the current study (38). 
 It is also possible that niacin's clinical benefit may result not from its lipid effects, but rather may be contingent on any of its several reported pleiotropic properties. As such, consideration should also be paid to expanding data delineating the various nonlipoprotein-mediated effects of niacin as a means to explain its efficacy. Niacin has been documented to exhibit anti-inflammatory properties as evidenced by a reduction in lipoprotein-associated phospholipase A2 and C-reactive protein (38), suppress pro-atherogenic chemokines (39), and augment serum concentration of the atherprotective hormone adiponectin ((40),41), each of which could confer cardiovascular protection.

Importantly, decades of clinical data have confirmed the overall safety of niacin therapy, particularly that of the prescription version used in the AIM-HIGH study. A recent review of the U.S. Food and Drug Administration's (FDA) Adverse Event Reporting System found prescription niacin to be associated with a lower rate of serious adverse events (defined as resulting in hospitalization or death), hepatotoxicity, and rhabdomyolysis compared with that of several other commonly used lipid-altering drugs including simvastatin, pravastatin, atorvastatin, gemfibrozil, and fenofibrate (48). Furthermore, the safety profile of niacin-statin combination therapy has been found comparable to that of either drug alone ((48),(49),50).


Sunday, December 22, 2013

Slide presentation of my case study

Slideshow of Tubby Traveler from Topekahttps://docs.google.com/presentation/d/1wf8eaZwoJTPpng4dKS6p3vyj7cQNRgWJGK6uNdxfG0U/edit

Go to the above site to see my slide presentation of my case study.  Extensive lab documents available for lipid geeks.

This is only a case study of one but I show the results of routine lipid panel, VAP, Liposcience and Berkley Heart lab while on a diet consisting of 60% fat, mostly animal fat over the course of 2011.

The co-variable of weight loss was not responsible as I did not lose weight. 
I exercised two to three hours a day in 2010.  In 2011, I decreased my exercise to an average of walking 40 minutes a day.
I stayed on crestor, niacin and lovaza as I had for years.  I did not increase the doses.
I don't think I have good genetics.  I have diabetes and the genetic profile from Berkley Heart Lab is not especially good.  I am Apo E 3/4.

Saturday, December 21, 2013

Reduced obese is why we don't maintain weight loss


This link has an excellent 1 min 40 second video explaining that two people who weigh the same don't burn calories the same if one of them has lost weight and one has not.

Read my free manuscript to learn more details about the reduced obese, energy gap and the Sponge syndrome.

The free slideshow is faster:

Wednesday, December 18, 2013

Evidence not strong for fatty acids causing inflammation

Modulation of obesity-induced inflammation by dietary fats: mechanisms and clinical evidence

Kim-Tiu Teng, Chee-Yan Chang, Lin Faun Chang and Kalanithi Nesaretnam

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Nutrition Journal 2014, 13:12  doi:10.1186/1475-2891-13-12
Published: 29 January 2014

Abstract (provisional)

Obesity plays a pivotal role in the development of low-grade inflammation.
 Dietary fatty acids are important modulators of inflammatory responses.
 Saturated fatty acids (SFA) and n-6 polyunsaturated fatty acids (PUFA) have been reported to exert pro-inflammatory effects. 
n-3 PUFA in particular, possess anti-inflammatory properties. 
Numerous clinical studies have been conducted over decades to investigate the impact of dietary fatty acids on inflammatory response in obese individuals, however the findings remained uncertain. 

High fat meals have been reported to increase pro-inflammatory responses, however there is limited evidence to support the role of individual dietary fatty acids in a postprandial state.

 Evidence in chronic studies is contradictory, the effects of individual dietary fatty acids deserves further attention. 
Weight loss rather than n-3 PUFA supplementation may play a more prominent role in alleviating low grade inflammation.
 In this context, the present review provides an update on the mechanistic insight and the influence of dietary fats on low grade inflammation, based on clinical evidence from acute and chronic clinical studies in obese and overweight individuals.

The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production

Tuesday, December 10, 2013

From Harvard School of Public Health

It’s Time to End the Low-Fat Myth



One highly-publicized report analyzed the findings of 21 studies that followed 350,000 people for up to 23 years. Investigators looked at the relationship between saturated fat intake and coronary heart disease (CHD), stroke, and cardiovascular disease (CVD). Their controversial conclusion: “There is insufficient evidence from prospective epidemiologic studies to conclude that dietary saturated fat is associated with an increased risk of CHD, stroke, or CVD.”(21)

With headlines like “Saturated Fat is Not Your Heart’s Enemy,” and “NOT GUILTY: The Long-Standing Vilification of Saturated Fat Finally Turning to Vindication,”(23,24) some of the media and blog coverage of these studies would have you believe that scientists had given a green light to eating bacon, butter, and cheese. But that’s an oversimplified and erroneous interpretation. Read the study and subsequent studies more closely, and the message is more nuanced: Cutting back on saturated fat can be good for health if people replace saturated fat with good fats, especially, polyunsaturated fats. (16,25)  Eating good fats in place of saturated fat lowers the “bad” LDL cholesterol, and it improves the ratio of total cholesterol to “good” HDL cholesterol, lowering the risk of heart disease. Eating good fats in place of saturated fat can also help prevent insulin resistance, a precursor to diabetes. (26)
Cutting back on saturated fat will likely have no benefit, however, if people replace saturated fat with refined carbohydrates—white bread, white rice, mashed potatoes, sugary drinks, and the like.

21. Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010;91:535-46.

My case study documented in my book, The Tubby Traveler from Topeka,  replaces carbs with mostly animal fat.  I eat bacon, sausage and steak 3-5 times a week.  I eat three eggs at least five times a week.  My CIMT is stable, my LDL-P is < 1,000.  Harvard makes the mistake of not using LDL-P instead of LDL-C.

See a longer summary of the article and my comments at: