6.5 minute video on why you can't maintain weight loss and what to do about it

Why you can't maintain weight loss link


A normal person has 40 billion fat cells.

An obese person has 120 billion fat cells. 

A reduced obese person has 120 billion shrunken fat cells. 

Those shrunken fat cells are the SPONGE to soak up calories and why you can't maintain weight loss. 

I call it the Sponge Syndrome of the Reduced Obese.

My recent writtings 2014

My Commentary on Lecture Pad link

Commentary by Brian Edwards, MD regarding the manuscript: Diets to Prevent Coronary Heart Disease 1957- 2013: What Have We Learned?By James E. Dalen, MD, MPH and Stephen Devries, MD, FACC from the American Journal of Medicine

You have to register on Lecture Pad to read article or you can read it on my documents: https://docs.google.com/document/d/1u6OtjPONyBVmlB1mXVsRSdwWKpTnZTuWcF31TyI3W50/edit


I review 3 articles by Yale Professor Katz 

Why people can't maintain weight loss

http://t.co/fQNDNVXe

Watch the 1 min 40 sec video below to understand why people who have lost weight almost always gain it back. 

  Dr. Rudolph Leibel and Dr. Michael Rosenbaum, have been researching the effects of the hormone leptin on weight maintenance.

Giants of Obesity Reseach

Glycemic index- Brazilian bean study

Market in Belum, Brazil
(Am. J Clin Nutr 2007; 86(3): 707-13. This was an eighteen-month randomized trial of a low-glycemic index diet and weight change in Brazilian women. Two hundred eight women were on two diets with 41-point difference in glycemic index. They did not have a significant difference in weight loss. No differences in hunger. To replace fat with fruits and vegetables does not seem to make a difference [as opposed to sugar and refined carbohydrates].)

A low glycemic might be defined as < 50

 Potato, white, baked in skin 85
Whole wheat bread (one slice) 77
Bran flakes cereal 74

Popcorn, microwaved 72 Pineapple, diced 66 Oatmeal instant, cooked 66 Raisins 64

Beets, canned 64
Figs, dried 61
Corn, sweet, boiled 60
Granulated table sugar (sucrose) 68 Brown sugar 59

Kiwi fruit 58 Apricots 57 Banana 52

I tried to eat healthy, by eating: Apples 38
Avocados 0
Cherries, sweet with pits 22 Grapes, green 46

Pears 38

(I ate fruit every day. I had a salad every day with Newman’s balsalmic vinaigrette. I gained 58 lbs. over four years despite two hours of exercise

CAC is the most robust test today to reclassify individuals risk for heart disease. Dr. Budoff

Screening for Heart Disease

By Matthew J. Budoff, MD, FACC

Matthew J. Budoff, MD, FACC

Professor of Medicine

David Geffen School of Medicine

Director of Cardiac CT

Harbor-UCLA Medical Center

Torrance, CA

Cardiovascular disease remains the leading cause of mortality in the U.S. and worldwide, and no widespread screening for this number one killer has been implemented.

Traditional risk factor assessment does not fully account for the coronary risk and underestimates the prediction of risk even in patients with established risk factors for atherosclerosis.

Coronary artery calcium (CAC) represents calcified atherosclerosis in the coronary arteries, and has been shown to be the strongest predictor of adverse future cardiovascular events. CAC consistently outperforms traditional risk factors, inflammatory biomarkers, and other tests of atherosclerosis such as carotid intimal media thickness (CIMT), endothelial function, and ankle-brachial index to predict future CV events.

It (CAC) has been incorporated into both the European and American guidelines for risk assessment.

CAC is the most robust test today to reclassify individuals based on traditional risk factor assessment and provides the opportunity to better strategize the treatments for these subjects (converting 77% of patients from intermediate risk to either high or low risk).

The risk for future adverse cardiovascular events increases with increasing CAC scores; however, the absence of CAC presents a very unique situation that is associated with very low risk status for the individual (10-year event rate of ~1%). It has been proposed that those without calcification may be at such a low risk status that further intervention with pharmacology may be unnecessary. The absence of CAC is associated with a very low risk of future cardiovascular events, presence of severe CAD, myocardial perfusion abnormalities, as well as likelihood of ACS.

The cumulative data provides strong confirmatory evidence that CAC is a strong predictor of events and that as radiation doses are being reduced to a minimum, may be a useful tool in the prevention of armamentarium to assess atherosclerosis progression non-invasively.

Based on available published evidence, CAC has been incorporated into the ACC/AHA guidelines for screening of asymptomatic individuals for CVD.

In this guideline, the cutpoint for CAC is >300, but this is too high a threshold for a score.

The MESA study demonstrated

1- a tenfold increased risk for calcium scores >100 and

2- a 14-fold increase for scores >300.

Both are at increased CV risk and both should be treated aggressively.

All other prospective studies (St Francis, Heinz-Nixdorff Recall Study, Dallas Heart, Rotterdam, and others)

demonstrate that 100 is an important cutpoint for increased CV risk.

Four years later, prominant Cardiologist echos my Tubby Theory message

This is a great video.  Dr. Seth Baum's Interventional prevention video

It is a scientific version of my 2010 video on how to prevent heart disease

This is a tremendous validation of the Tubby Theory from Topeka that I wrote in 2009 published in 2010.

I used Dr. Seth's metrics for the last four years to prove that a 60% fat diet does not make cause tremendous plaque build up. 

My lab and CIMT metrics 

I have not seen detailed follow up CIMT's in any other diet case.

Canadian update on risk stratification

Abstract 

Decisions for statin therapy in the primary prevention of atherosclerotic cardiovascular disease (ASCVD) are generally made using the 10-year Framingham risk score (FRS).

Even when a family history of premature CVD is taken into account, there is often ambiguity about the need for statin therapy for patients with a 10 year FRS of 5-19% and LDL C < 3.5mmol/l (135 mg/dl).

 Current Canadian dyslipidemia guidelines recommend consideration of a diversity of other factors, including biochemical measurements and imaging studies to help determine whether the calculated FRS may be misleadingly low and whether statin therapy might, therefore, be prudent.

 However, efficient utilization of the plethora of secondary factors makes this decision process itself potentially ambiguous.

This brief summary provides a practical approach for utilizing clinical information, basic biochemical tests and more specialized test, such as carotid ultrasound and coronary artery calcium scoring to identify groups of patients at higher risk for ASCVD than suggested by FRS.

Identification of patients at increased risk of ASCVD yet with an intermediate Framingham risk score (FRS) of 5-19% is enhanced by considering other medical issues and by secondary testing.

 A structured approach to the evaluation of intermediate FRS patients is presented. Using such a strategy it is likely more patients who will benefit from statin therapy will be initiated on treatment.

Experts: We may have been wrong about the evils of saturated fats

People should still avoid artificial trans fats, report says

11:43 AM - March 18, 2014

Saturated fat—the kind found in meat, cheese, and butter—may not increase one's risk of heart attack, according to a report in the Annals of Internal Medicine that challenges long-held beliefs about "good fats" and "bad fats."
For the report, researchers from Cambridge University and the British Heart Foundation analyzed data on more than 600,000 adults participating in 72 studies. They found that the participants' total saturated fat quantity—whether measured in their bloodstream or in their diet—had no effect on their risk of coronary disease.
Health experts have long warned against eating saturated fats because they have been linked to an increase in low-density lipoprotein (LDL) cholesterol—the kind that raises the risk of heart attacks. But researchers found that the relationship between LDL cholesterol and saturated fats is complex.
Although saturated fats cause an increase in LDL levels, 
they also increase high-density lipoprotein (HDL) levels. 
And the LDL that it does increase in a subtype is generally considered benign.

 Research suggests that it is actually sugary and carbohydrate-laden foods that increase the dangerous LDL types.
"It's the high carbohydrate or sugary diet that should be the focus of dietary guidelines," says lead author Rajiv Chowdhury, adding,
 "These are interesting results that potentially stimulate new lines of scientific inquiry and encourage careful reappraisal of our current nutritional guidelines."

Evidence that low carbohydrate diet does burn more calories?

"Despite consuming the same number of calories on each diet, subjects burned about 325 more calories per day on the low carbohydrate than on the low fat diet — amounting to the energy expended in an hour of moderately intense physical activity."

1-Sea change in Media coverage of low carb diets link

 2-Compare with Media coverage of this data in 2012 when it first came out link

 3-Compare media reviews of The Men Who Made Us Fat BBC documentary Link


Viewpoint | May 16, 2014

Increasing Adiposity Consequence or Cause of Overeating?

David S. Ludwig, MD, PhD^1,2; Mark I. Friedman, PhD³

^{JAMA article link} 

• 

How bad science started a war against saturated fats

When Americans ditched saturated fats, they embraced carbs

12:07 PM - May 8, 2014

Writing in the Wall Street Journal this week, nutrition expert Nina Teicholz explains why Americans came to misguided fears of saturated fats—like those in butter, cheese, and meat.
Her article comes on the heels of a report finding that the fats do not increase one's risk of heart attack.

How did we get here?

Although there has never been any "solid evidence" to support the theory, it has been generally accepted that saturated fats clog arteries.
 This theory comes from a "mixture of personal ambition, bad science, politics, and bias," Teicholz writes.

In the 1950s, University of Minnesota scientist Ancel Benjamin Keys began championing the idea that saturated fats raise bad cholesterol levels and, as a result, cause heart attacks. The country was struggling with a fast-growing epidemic of heart disease, and his theory fell on receptive ears, Teicholz writes. In 1961, Keys gained a seat on the American Heart Association's nutrition committee and that year the group issued the nation's first-ever recommendations targeted at reducing saturated fats consumption.
Shortly after, several studies touted the benefits of consuming vegetable oil—corn or soybean, but not olive—over animal fats, such as butter. Teicholz notes that the studies had "serious methodological problems," including not taking into account patients who smoked, but the bias had grown in "common sense."

Dealing with the consequences

As a result, Americans began replacing foods they believed high in saturated fats—meat, eggs, and cheese with carbohydrates—grains, pasta, fruit, and potatoes.

While saturated fat consumption dropped by 11%, carbohydrate consumption has increased by at least 25% since the early 1970s, Teicholz writes.

Even seemingly healthy foods such as low-fat yogurt became less healthy as manufacturers replaced fats with carbohydrate-based fillers to make up for the lost texture.

When carbohydrates break down into glucose, the body releases insulin and stores fat, which can lead to obesity, Type 2 diabetes, and cardiovascular disease.

 So, while Americans were trying to avoid heart conditions, they actually put themselves at a higher risk for them, Teicholz writes.

"The reality is that fat doesn't make you fat or diabetic.

 Scientific investigations going back to the 1950s suggest that actually, carbs do," Teicholz writes.

Another consequence of the saturated fats scare is that Americans began consuming more vegetable oils, margarine, and Crisco. Some studies have linked the consumption patterns with higher rates of gallstones and cancer.

"It is time to put the saturated fat hypothesis to bed and to move on to test other possible culprits for our nation's health woes," Teicholz writes (Teicholz, Wall Street Journal, 5/6).

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Historic NLA meeting in Orlando going over new LIPID guidelines.

Posted 5-4-14

Grundy, Stone and V Brown were all on the first ATP I guideline committee 25 years ago.  Neil Stone was the new chairman of the ACA/AHA 2014 lipid guidelines that recently came out.  He received a good deal of criticism because he (the committee)  advised giving statins sooner at a 7.5% risk over 10 years.  He created a risk estimator that improves on the old Framingham risk calculator.

Dr. Neil Stone said the initial criticisms of his estimator have proven unfounded as well as the fact that 7.5% risk does not mean automatic statin but instead automatic discussion between the Doctor and the patient about the patients options.

If a patient is uncertain a CAC (Coronary Calcium Score) can then be done to see if a CAC 300 reclassifies the patient to a higher risk category.  

If the CAC is zero, then the patient can be reclassified to low risk and not go on statin for 5 years and then repeat CAC.  

Atorvastatin 20 mg is considered a moderate dose & could be advised to be given even with a very low risk of 5% over 5 years.  But Stone and committee decided to be conservative and put the cut off higher at 7.5%.

The NLA published a draft of it's own recommendations on Fri that was more patient centered than population centered to fill out some gaps of the ACA/AHA guideline.

CAC maven Dr. Matthew Budoff believes the cut-off to re-classify patients from intermediate risk to high risk should be CAC 100 or higher.

Budoff said if you have a CAC of 100 you have 10 fold increased risk of Cardiovascular event.

Both guidelines agree that 10 year risk should be replaced with lifetime risk till age 80.  A diabetic age 50 would have about a absolute lifetime risk of 60%.

Atorvastatin 20 mg is a moderate dose but if given over a longer period at an earlier stage progression of atherosclerosis can be stopped.

I believe rather than doubling Atorvastin if follow up lab does not reach threshold (as opposed to goals?) which would only decrease LDL-C by 6% more,

I believe adding wax matrix niacin 1,000 mg a day achieves 16% LDL-C reduction (As per COMPELL trial) and as with many combination models of treatment in medicine, lower dose meds with different actions causes less side effects especially for lifetime treatment.

NLA recommendations are not superior to ACA/AHA guidelines as the NLA is using more data other than Random Controlled Trials.  It tries to use more data to have more flexibility at the patient level.  Dr. Stone argued he used data before 1995 such as Helsinki when evaluating non-statin therapy.  He also used data after 2012 such as REGARD when evaluating the risk estimator.

Stone insists his guidelines state that the decision to start statin occurs only after a discussion of options with the patients. Dr. Stone said the media missed this point and misrepresented the guidelines in that regard as well as follow up lab work.

Both groups agree that non-HDL cholesterol should replace LDLc as a better predictor of risk.  I predicted that change in my Tubby Theory book from 2009.

Both groups agree that lifestyle changes should precede statin most of the time.  Mediterrannean diet was advised as the best and least restrictive as it allows a full range of food.  I think it is still restrictive as you have to move to the Mediterranean area to get the true non-stress life that is an important confounding co-variable.

However for weight loss, any diet the patient can stay on is the best diet.  

I think the guidelines need to warn patients of the reduced obese state.  Once you lose 10% or more weight on a 1500 calorie diet, you need to stay on the 1500 calorie diet the rest of your to maintain your weight loss.

See http://t.co/fQNDNVXe