How to maintain weight loss 6 min video

One minute 40 second video on why we regain our weight loss

HBO Weight Loss Nation link


The above video shows why the reduced obese regain their weight.

Someone who has lost more than 10% of their body weight will always have to eat 20% less than someone the same weight who has never been on a weight loss diet.

Bottom line: You need to stay on a low calorie diet (sub-starvation) the rest of your life to maintain your weight loss.

Exercise metabolism is reduced in the reduced obese.

Metabolism decreases 2% every decade.

June 2014 on Tubby Theory- youtube 6 min 40 sec video

More validation of Tubby Theory and Multiplier effect Update 2015

PCSK9FORUM Education and Research

More validation of Tubby Theory and Multiplier effect

From article below:

“Thus carotid intima-media thickness (CIMT)seems to work in younger individuals13

where calcified plaques are rare

whereas coronary artery calcium(CAC) identifies older high-risk subjects14 .”

Lifetime exposure and primordial prevention

Posted by Anthony Wierzbicki | Posted in From the Editors

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Atherosclerosis is a slow onset insidious disease. It is asymptomatic until its manifestations cause significant morbidity and mortality. There is no cheap easy way to detect it. As a result disease management strategies rely on epidemiologically-based risk calculators to identify individuals likely to have significant disease1 .

The greatest contribution to cardiovascular disease (CVD) risk is age rather than risk factors and some advocate treatment strategies simply based on this criterion to minimise health expenditure2 .

Everyone in cardiovascular prevention clinics is familiar with patients with isolated high cholesterol secondary to menopause or hepatic steatosis secondary to carbohydrate-rich diets where the diagnosis is often made by reference to a previous cholesterol result taken a few years ago.

What actually counts for all risk factors is not only their level but the years of exposure to the risk factor.

Epidemiological studies have repeatedly used smoking-pack-years3 and diabetes-years4 as prognostic indices that offer advantages over dichotomous distributions or single point levels.

This is also a feature for cholesterol and hypertension exposure and has been recorded as such in studies such as Framingham for surrogate outcomes such as carotid stenosis5 .

Cholesterol-years exposure neatly explains the epidemiology of CVD risk in familial hypercholesterolaemia6 .

A recent paper has brought this ancient insight back into focus by analysing the Framingham Offspring Cohort and showing that time-integrated cholesterol exposure is a strong predictor of future CVD events7 .

After15 years of follow-up coronary heart disease rates were 4.4% for those with no exposure prior to age 55 years, 8.1% for those with 1-10 years and 16.5% for those with 11-20 years exposure. Many of those with prolonged exposure would not have been identified by current CVD risk calculators.

The CVD risk calculator approach has its flaws and some have proposed lifetime risk as superior to 10-year risk as a better way of identifying high risk individuals in any age cohort8 9 .

Yet most lifetime risk calculation systems rely on single point measures from cross-sectional studies extrapolated to longitudinal conclusions10 . What is actually required is integrated risk exposure11 .

Electronic health record systems and systematic screening programmes are gathering the data to allow exposures to be adequately calculated. All the CVD risk factor calculation algorithms will require updating with this data, and more difficult, adequate validation. Alternatively a mechanism is required that integrates cholesterol exposure analogous to diabetes–years and HbA1c for glucose.

Modern imaging techniques can identify subsets of individuals who classical risk factors miss12 .

Thus carotid intima-media thickness (CIMT)seems to work in younger individuals13

where calcified plaques are rare

whereas coronary artery calcium(CAC) identifies older high-risk subjects14 .

   

This insight about cholesterol exposure suggests a number of approaches to intervention. Early intervention with small changes could translate into profound later benefits- the doctrine of primordial prevention17 . A 0.6mmol/L reduction in LDL-C at age 50 could reduce CVD events by 39%; while at age 70 a 1.4 mmol/L reduction is required to achieve similar benefit15 . The current debates about guidelines and their reduced intervention thresholds are in many ways arguments about which strategy is better in early middle age. What is required in populations over the long-term is a change of lifestyles to increase physical activity, reduce weight and banish smoking. That will take considerable time. In the interim medical intervention will be required in high risk groups if these can be satisfactorily and cost-effectively identified16 .

Contact details: Prof Anthony S. Wierzbicki DM, DPhil, FRCPath

Department of Chemical Pathology

St Thomas Hospital

Lambeth Palace Road

London SE1 7EH UK

E-mail: Anthony.Wierzbicki@kcl.ac.uk

ent TH. Predicting the risk of coronary heart disease I. The use of conventional risk markers. Atherosclerosis 2010; 213: 345-51.
2.	⇧	Wald NJ, Simmonds M, Morris JK. Screening for future cardiovascular disease using age alone compared with multiple risk factors and age. PLoSOne 2011; 6: e18742.
3.	⇧	Howard G, Wagenknecht LE, Burke GL et al. Cigarette smoking and progression of atherosclerosis: The Atherosclerosis Risk in Communities (ARIC) Study. JAMA 1998; 279: 119-24.
4.	⇧	Nathan DM, Lachin J, Cleary P et al. Intensive diabetes therapy and carotid intima-media thickness in type 1 diabetes mellitus. NEnglJ Med 2003; 348: 2294-303.
5.	⇧	Wilson PW, Hoeg JM, D’Agostino RB et al. Cumulative effects of high cholesterol levels, high blood pressure, and cigarette smoking on carotid stenosis. The New England journal of medicine 1997; 337: 516-22.
6.	⇧	Nordestgaard BG, Chapman MJ, Humphries SE et al. Familial hypercholesterolaemia is underdiagnosed and undertreated in the general population: guidance for clinicians to prevent coronary heart disease: consensus statement of the European Atherosclerosis Society. Eur Heart J 2013; 34: 3478-90a.
7.	⇧	Navar-Boggan AM, Peterson ED, D’Agostino RB, Sr. et al. Hyperlipidemia in early adulthood increases long-term risk of coronary heart disease. Circulation 2015; 131: 451-8.
8.	⇧	Lloyd-Jones DM, Leip EP, Larson MG et al. Prediction of lifetime risk for cardiovascular disease by risk factor burden at 50 years of age. Circulation 2006; 113: 791-8.
9, 10.	⇧	Hippisley-Cox J, Coupland C, Robson J, Brindle P. Derivation, validation, and evaluation of a new QRISK model to estimate lifetime risk of cardiovascular disease: cohort study using QResearch database. BMJ 2010; 341: c6624.
11.	⇧	Martin SS, Michos ED. Mapping hyperlipidemia in young adulthood to coronary risk: importance of cumulative exposure and how to stay young. Circulation 2015; 131: 445-7.
12.	⇧	Erbel R, Budoff M. Improvement of cardiovascular risk prediction using coronary imaging: subclinical atherosclerosis: the memory of lifetime risk factor exposure. Eur Heart J 2012; 33: 1201-13.
13.	⇧	Ratchford EV, Carson KA, Jones SR, Ashen MD. Usefulness of coronary and carotid imaging rather than traditional atherosclerotic risk factors to identify firefighters at increased risk for cardiovascular disease. The American journal of cardiology 2014; 113: 1499-504.
14.	⇧	Nasir K, Rubin J, Blaha MJ et al. Interplay of coronary artery calcification and traditional risk factors for the prediction of all-cause mortality in asymptomatic individuals. CircCardiovascImaging 2012; 5: 467-73.] and convincingly adds to classical CVD risk factors in predicting disease[Kavousi M, Elias-Smale S, Rutten JH et al. Evaluation of newer risk markers for coronary heart disease risk classification: a cohort study. AnnInternMed 2012; 156: 438-44.
15.	⇧	Law MR, Wald NJ, Rudnicka AR. Quantifying effect of statins on low density lipoprotein cholesterol, ischaemic heart disease, and stroke: systematic review and meta-analysis. BMJ 2003; 326: 1423.
16.	⇧	Sniderman AD, Thanassoulis G, Lawler PR et al. Comparison of coronary calcium screening versus broad statin therapy for patients at intermediate cardiovascular risk. AmJ Cardiol 2012; 110: 530-3.
17.	⇧	Robinson JG, Gidding SS. Curing atherosclerosis should be the next major cardiovascular prevention goal. Journal of the American College of Cardiology 2014; 63: 2779-85.

   

Validation of Sponge Syndrome

I developed the idea of the Sponge Syndrome explaining why the reduced obese could not maintain weight loss when I was at the Mall of America in 2011 and saw a statue of Square Pants Sponge Bob.

My 6.5 minute video 

Thanks to

Christopher N Ochner

Adam G Tsai

Robert F Kushner

Thomas A Wadden

and The Lancet Diabetes and Endocrinology publication. 

Ochner et al article Feb 11, 2015 link

"Many clinicians are not adequately aware of the reasons that individuals with obesity struggle to achieve and maintain weight loss,1 and this poor awareness precludes the provision of effective intervention.2

Irrespective of starting weight, caloric restriction triggers several biological adaptations designed to prevent starvation.3

These adaptations might be potent enough to undermine the long-term effectiveness of lifestyle modification in most individuals with obesity, particularly in an environment that promotes energy overconsumption.

However, they are not the only biological pressures that must be overcome for successful treatment.

Additional biological adaptations occur with the development of obesity and these function to preserve, or even increase, an individual's highest sustained lifetime bodyweight.

For example, preadipocyte proliferation occurs, increasing fat storage capacity."

In addition, habituation to rewarding neural dopamine signalling develops with the chronic overconsumption of palatable foods, leading to a perceived reward deficit and compensatory increases in consumption.4

Importantly, these latter adaptations are not typically observed in individuals who are overweight, but occur only after obesity has been maintained for some time.3

Thus, improved lifestyle choices might be sufficient for lasting reductions in body weight prior to sustained obesity.

Once obesity is established, however, body weight seems to become biologically stamped in and defended.

Therefore, the mere recommendation to avoid calorically dense foods might be no more effective for the typical patient seeking weight reduction than would be a recommendation to avoid sharp objects for someone bleeding profusely.

Evidence suggests that these biological adaptations often persist indefinitely, even when a person re-attains a healthy BMI via behaviourally induced weight loss.3

Further evidence indicates that biological pressure to restore body weight to the highest-sustained lifetime level gets stronger as weight loss increases.5

Thus, we suggest that few individuals ever truly recover from obesity; individuals who formerly had obesity but are able to re-attain a healthy body weight via diet and exercise still have ‘obesity in remission’ and are biologically very different from individuals of the same age, sex, and body weight who never had obesity.3, 5

For most individuals, these biological adaptations need to be addressed for weight loss to be sustained long-term.

We believe these mechanisms largely explain the poor long-term success rates of lifestyle modification, and obligate clinicians to go beyond mere recommendations to eat less and move more.

8 year weight loss maintenance of 5% failed to improve CV outcomes

Why this Low-fat diet failed 

The LOOK AHEAD trial failed in its primary outcome NEJM July 11, 2013.

However secondary outcomes at 5% weight loss  were good.  2014 Dec  Pi-Sunyer X1.

The LOOK AHEAD trial is one of the longest diet studies on record.

The average BMI was 35?  Healthy weight is up to 24.9 BMI?

At 5 ft 6 inches someone 220 lbs has a BMI of 36.

5% of 220 = 11 lbs.

220-11= 209 lbs

The BMI is now 34.

Average weight loss was 5% .

I suggest LOOK AHEAD failed it's primary outcome because 5% was insufficient weight loss

My main concern is that this patient needs and wants to get to a healthy BMI of 24 by achieving a weight of 150 pounds.

That is a 70 pound weight loss or 31% weight loss.

I found this subgroup fact from Medscape Jan 2014 : "11% of the Intensive therapy group maintained 15% weight loss after 8 years"

This is the subgroup which I wonder if they had a positive primary outcome.  

The challenge in obesity is to maintain a 30% weight loss to maintain a healthy BMI for more than five years and perhaps no longer need diabetic medication.  I am not clear as to whether Bariatric surgery has achieved this.

This HBO Weight Nation 2 min video is the real challenge for the reduced obese who lose more than 8-10% of body weight.

Nation Weight Control Registry has 10,000 people who have achieved this weight loss maintenance.  This is how they do it : NCWR weight loss method

The people in NWCR did it on their own? without monthly counseling?  Very special self selected group of people.

The ILI (treatment) arm group of people probably comes close to the NWCR groups dedication.

I asked my son if he was fat and I told him to keep 5% of his weight off for 8 years he would have to have monthly counseling sessions, keep a food diary, exercise for an hour a day and eat 1200 to 1500 calories a day only to maintain that weight loss, would he do it?

He said “maybe”.

Then I said, LOOK AHEAD shows if you do all that you still only have 11% chance of success.

He said, “no it seems like too much trouble.”

More discussion at: LOOK AHEAD trial articles

Hunger Games Lecture at NOLA NLA meeting

My slideshow is available at:

https://docs.google.com/presentation/d/1Q5qZs6KbwirZMagCiSJ10zrbc2V_BkG_QVN4oKDqaBo/edit#slide=id.gac7b8f7f_017

Objective: What to do when you hit the plateau of dieting.

HDL-P is superior to HDL-C in predicting prevalent atherosclerosis as well as incident CHD events across a diverse population and should be considered as a therapeutic target.

Therapies targeting high-density lipoprotein cholesterol content (HDL-C) have not improved coronary heart disease (CHD) outcomes.
High-density lipoprotein particle concentration (HDL-P) may better predict CHD.

 However, the impact of race/ethnicity on the relations between HDL-P and subclinical atherosclerosis and incident CHD events has not been described.

Participants from the Dallas Heart Study (DHS), a multiethnic, probability-based, population cohort of Dallas County adults, underwent the following baseline measurements: HDL-C, HDL-P by nuclear magnetic resonance imaging, and coronary artery calcium by electron-beam computed tomography.

Participants were followed for a median of 9.3 years for incident CHD events (composite of first myocardial infarction, stroke, coronary revascularization, or cardiovascular death).

 The study comprised 1,977 participants free of CHD (51% women, 46% black). In adjusted models, HDL-C was not associated with prevalent coronary artery calcium (p = 0.13) or incident CHD overall (hazard ratio [HR] per 1 SD 0.89, 95% confidence interval [CI] 0.76 to 1.05).

However, HDL-C was inversely associated with incident CHD among nonblack (adjusted HR per 1 SD 0.67, 95% CI 0.46 to 0.97) but not black participants (HR 0.94, 95% CI 0.78 to 1.13, p_interaction = 0.05).

 Conversely, HDL-P, adjusted for risk factors and HDL-C, was inversely associated with prevalent coronary artery calcium (p = 0.009) and with incident CHD overall (adjusted HR per 1 SD 0.73, 95% CI 0.62 to 0.86), with no interaction by black race/ethnicity (p_interaction = 0.57).

In conclusion, in contrast to HDL-C, the inverse relation between HDL-P and incident CHD events is consistent across ethnicities.

 These findings suggest that HDL-P is superior to HDL-C in predicting prevalent atherosclerosis as well as incident CHD events across a diverse population and should be considered as a therapeutic target.

Amer Jour Cardio