Tag: diet

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Weight loss and blood pressure


Hmm, that’s an interesting question. When I counsel patients on controlling blood pressure I mention weight loss but don’t perseverate on it because of the general futility of of achieving lasting weight loss. Most diets deliver only modest weight loss and that weight loss is depressingly short lived:
The figure above is the primary results from a trial of various strategies to preserve weight loss. 1,685 patients were enrolled, only 1,032 lost the require 10 lbs to begin Phase 2. In Phase 2 patients were randomized to 1) minimal intervention 2) web-based interaction 3) monthly contact with an interventionist. Patients with monthly contact regained 3 lbs less than the patients with self-directed maintenance. Svetkey et al. Comparison of strategies for sustaining weight loss: the weight loss maintenance randomized controlled trial. JAMA (2008) vol. 299 (10) pp. 1139-48 (PDF)

Second study looking at Weight Watchers compared to a self-help program for weight loss. Same pattern, modest weight loss followed by rebound to regain much of the lost weight. Heshka et al. Weight loss with self-help compared with a structured commercial program: a randomized trial. JAMA (2003) vol. 289 (14) pp. 1792-8 (PDF)

I focus my limited office time on changing patients’ diet to reduce blood pressure. I recommend the DASH diet (PDF) to all of my patients without significant metabolic bone disease or hyperkalemia because I believe the data shows that it is the most effective life-style intervention to ameliorate hypertension. Unfortunately those two exclusions (bone disease and potassium) exclude many of my patients. I usually don’t recommend the low sodium version of of DASH because I feel that the reduction in palatability is not supported by the rather modest additive effects (an additional 3 mmHg reduction in SBP). Most of my patients recognize that they eat too much and have been trying to reduce calories, and lose weight for years prior to seeing me. I feel that by discussing the DASH diet and not rehashing the same tired dietary advice that every doctor has been promoting, I provide them with a novel view of dietary changes that they are willing to try.

Still, I think The Kidney Group has an interesting question, what is more important weight loss or diet changes?

NephSAP recently reviewed hypertension. On page 98 they had this table which compared various lifestyle interventions and their effect on blood pressure:
Unfortunately they grouped diet and weight loss in one group so it does not allow me to separate out the effect of changing diet from changing weight. Regardless, the effect on blood pressure looks modest compared to the findings of the DASH diet or DASH sodium intervention. From the abstract of the DASH-Sodium trial (PDF):

As compared with the control diet with a high sodium level, the DASH diet with a low sodium level led to a mean systolic blood pressure that was 7.1 mm Hg lower in participants without hypertension, and 11.5 mm Hg lower in participants with hypertension.

The Archive published this meta-analysis (PDF) in 2008 looking at weight loss by diet or drugs with respect to mortality and blood pressure control.


They found that weight loss did result in blood pressure reductions but the reduction was modest. Additionally not all methods were equal, with silbutamide (Meridia) resulting in an increase in blood pressure despite being effective at reducing weight. They were unable to find any studies which showed a reduction in weight reducing mortality.

The above systemic review mentioned that the TONE study was one that was particularly well done. The TONE trial (PDF) was published in JAMA in 1998 and compared sodium restriction to weight loss to usual care in a two by two factorial design. The enrolled 585 obese patients to be randomized to either weight loss, no weight loss, salt restriction or not. Another 390 were randomized to either salt restriction or usual diet.
The investigators achieved nice separation of the groups with regard to weight loss. The study began with every patient weaning off their antihypertensive medication and the primary end-point was the fraction resuming their pharmacologic blood pressure medications and the time to resumption. Weight loss was more effective than no intervention and about equally efficacious as sodium restriction:

Note the lower starting blood pressure for sodium intake, this accounts for some of the difference in the effect on blood pressure.

Though TONE showed no difference between weight loss and sodium restriction, I feel that diet is probably more important because sodium restrictionis not the most effective dietary change to reduce blood pressure, the DASH diet is. I feel that if the TONE trial was rerun with the DASH diet replacing sodium restriction we might see that diet is more important than weight loss.

One thing I am doing in my clinic more and more is recommending bariatric surgery. Medical and behavioral changes have a poor track record at providing lasting and significant weight loss. Bariatric surgery shows lasting weight loss 10 years out and it allows patients to recover from hypertension and diabetes. Sjöström et al. Lifestyle, diabetes, and cardiovascular risk factors 10 years after bariatric surgery. N Engl J Med (2004) vol. 351 (26) pp. 2683-93. (PDF)

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Its not the sodium intake its the sodium:potassium ratio

Don’t worry only about sodium intake (NYC, I’m looking at you) and its not just potassium intake (DASH diet in the cross-hairs). It’s all about the sodium potassium ratio. This is shown by Cook et al (PDF). during reanalysis of the Trial of Hypertension Prevention I and II. This trial had serial 24-hour urine collections done in 2,275 patients with pre-hypertension in the late 80’s and 90’s. The investigators looked at that data through the lens of 15 years of follow-up to determine the risk of cadiovascular events:

In observational analyses of the mean urinary excretion during 11⁄2 to 3 years, we found a suggested positive relationship of urinary sodium excretion and a suggested inverse relationship of urinary potassium excretion with risk of CVD, but neither was statistically significant when considered separately. Both measures strengthened when modeled jointly, with opposite but similar effects on risk. However, the sodium to potassium excretion ratio displayed the strongest and statistically significant association, with a 24% increase in risk per unit of the ratio that was similar for CHD and stroke and was consistent across subgroups.

Here is the key figure. Note in the graph the rate of events is presented on a log scale so the 2 indicates a rate 100 times the rate at zero.

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Journal Club: low protein diet

Effect of a very low protein diet on outcome: long-term follow-up.

This is the long-term follow-up of the B group from the original MDRD study.
Enrollment criteria:
  • Age: 18-70
  • Abnormal Cr 1.2-7 women 1.4-7 in men.
  • MAP of 125 or less (160/100)
  • Proteinuria less than 10g per day
  • No diabetics
GFR 13-24 mL/min for the B study (low protein versus very low protein diet). Higher GFR were enrolled in the A study (normal protein versus low protein diet).
Protein was restricted for 3 years.
9 months after the study every nutritional parameter was the same between the two groups.

The primary end-point was a composite of death or dialysis and just about every patient in both groups (95.7%) reached this end-point preventing a separation between the groups (p=0.5). Likewise there was no separation with regards to time to dialysis (p=0.4).

The surprising finding occurs when they looked at death after the initiation of dialysis. There were 34 deaths in the very low-protein group and 19 deaths in the low-protein group (p=0.01).

The separation begins around 15 months and grows over time. This difference was statistically significant and grew to a 2-fold increased risk of death after 6 years.

My take is this fits well with what I tell my patients when they ask me about protein restriction. I have always counseled patients against protein restriction. The two largest RCT were both negative trials (The Modification of Diet in Renal Disease and the Northern Italian Cooperative Study Group). Additionally my patients do not have the benefit of dedicated and repeated nutritional couseling that the patients in these trials receive. My fear is that with little therapeutic upside there is signifigent risk of malnutrition from overzealous protein restriction.

This study probably does not apply to my worry as I doubt patients would adhere to a very low-protein diet.

My other concearn regarding low-protein diets is patients need to get calories from somewhere. Calories can only come from protein, carbohydrates or fat. Considering that the vast majority of CKD patients are destined to die before dialysis I worry that my advice for protein restriction will result in increased carbohydrates (bad for diabetes and possibly CV disease, see Richard Johnson’s fructose hypertension research) and/or increased fats (bad for CV disease) and enhance the risk of death from the more likely outcome.

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The fall of cholesterol

The cholesterol theory of heart disease has been getting knocked around a bit these days.

Just writing that sentence feels rebelous. To call cholesterol’s causative link with heart disease a theory seems blasphemous. I started thinking about this when I looked over some summaries of the Jupiter data.

The results of the JUPITER trial indicate that rosuvastatin is associated with a significant reduction in major cardiovascular events, including death, in apparently healthy persons with LDL cholesterol less than 130. The reduction in risk was roughly twice as high as one would predict from the reduction in the LDL:

Moreover, the results were quite different from those of trials that recruited on the basis of elevated LDL.

Those trials “generally reported a 20% reduction in vascular risk for each 1 mmol/L (38.7 mg/dL) absolute reduction in the LDL cholesterol level, an effect that would have predicted a proportional reduction in the number of events in our study of approximately 25%,” the investigators wrote.

“However, the reduction in the hazard seen in our trial, in which enrollment was based on elevated high-sensitivity C-reactive protein levels rather than on elevated LDL cholesterol levels, was almost twice this magnitude and revealed a greater relative benefit than that found in most previous statin trials,” they added.

This mismatch with reduction in LDL and reduction is risk is similar to the findings of with ezetimibe which showed no reduciton in the progression of atherosclerosis despite dramatic reductions in cholesterol.

Add to that the increase rather than reduction in first major cardiovascular events associated with torcetrapib which successfully increased HDL and reduced LDL. Another nail in the coffin also comes with torcetrapib which despite increasing HDL and reducing LDL failed to reduce atheroma volume.

It seems that large swaths of the cholesterol theory need to be revised and updated to account for this new data. While we wait for this new hypothesis it is important to reevaluate all of the conclusions and health recommendations we make based on intermediate end-points rather than on clinical outcomes. The primary health recommendations that I have in my sites are dietary. Low fat diets have repeatedly failed studies on endpoints and are propagated on their ability to improve the lipid profiles. Well, both ezetimibe and torcetrapib improve the lipid profiles and do little else of benefit to patients.

From a 2002 JAMA review:

In the Minnesota Coronary Survey,51 cardiovascular events were not significantly reduced by a high-polyunsaturated-fat diet despite a decrease in serum cholesterol, but the mean duration of dietary intervention was only about 1 year. Two secondary prevention trials testing the approach of total fat reduction did not find a significant reduction in serum cholesterol or CHD events.52–53

A more recent reveiw from Circulation comes to a similar conclusion. It reminds me of a NYT magazine article about the Atkins diet. This wonderful article has a section that looks at the lack of correlation between Heart Healthy diets and actually reducing cardiac events.

It began in January 1977, when a Senate committee led by George McGovern published its ”Dietary Goals for the United States,” advising that Americans significantly curb their fat intake to abate an epidemic of ”killer diseases” supposedly sweeping the country. It peaked in late 1984, when the National Institutes of Health officially recommended that all Americans over the age of 2 eat less fat. By that time, fat had become ”this greasy killer” in the memorable words of the Center for Science in the Public Interest, and the model American breakfast of eggs and bacon was well on its way to becoming a bowl of Special K with low-fat milk, a glass of orange juice and toast, hold the butter — a dubious feast of refined carbohydrates.

In the intervening years, the N.I.H. spent several hundred million dollars trying to demonstrate a connection between eating fat and getting heart disease and, despite what we might think, it failed. Five major studies revealed no such link. A sixth, however, costing well over $100 million alone, concluded that reducing cholesterol by drug therapy could prevent heart disease. The N.I.H. administrators then made a leap of faith. Basil Rifkind, who oversaw the relevant trials for the N.I.H., described their logic this way: they had failed to demonstrate at great expense that eating less fat had any health benefits. But if a cholesterol-lowering drug could prevent heart attacks, then a low-fat, cholesterol-lowering diet should do the same. ”It’s an imperfect world,” Rifkind told me. ”The data that would be definitive is ungettable, so you do your best with what is available.”