By George Henderson and Grant Schofield

There are few diet trials published from New Zealand, so we’re always keen to see them; and there are even fewer vegan diet trials.

We are even more interested when they go beyond their data, and start in on a sort of zealot approach to running down low carb diets which this study gives no insight into.

So what did they do? They went vegan (plant only) That is, we think this was a vegan study, because it’s called a “whole food plant based diet”, well-known vegan doctors are cited in the supplementary materials, dietary fat intakes were, though not measured, intended to be very low indeed, and because B12 supplements were supplied, but few details about the intervention are given, and even fewer about the controls; these received “standard medical care” with no diet advice mentioned.

The study was small (n=65) and not as representative as the authors might have hoped for; “The intervention involved patients from a group general practice in Gisborne, the region with New Zealand’s highest rates of socioeconomic deprivation, obesity and type 2 diabetes” – however, after randomisation there were only 3 Māori with 30 NZ European in the intervention arm (n=33) whereas the control arm had 21 European, 5 Māori and 6 other (n=32).

The results were excellent in terms of weight loss, and good in terms of medication reduction, with a couple of people reversing diabetes. Weight lost was as great as in the best ketogenic diet trials, although the controls here, with no diet change (or else useless advice based on NZ government recommendations? It would be good to know) provided no competition.

“The mechanism for this is likely the reduction in the energy density of the food consumed (lower fat, higher water and fibre). Multiple intervention participants stated ‘not being hungry’ was important in enabling adherence.” In other words, de facto calorie restriction is likely to have occurred, due to greater satiety per calorie, the same as mooted in LCHF studies.

The weight changes at 3 months don’t compare too badly with the weight changes at 10 weeks in the first report from this long term ketogenic diet study. [2] The reductions in medication and reversals of diabetes are greater in the ketogenic diet study, with a similar intensity of intervention, but nonetheless the BROAD weight loss results are very good by the standards of most diet trials.

So the Whole food plant-based (WFPB) diet didn’t do too badly for weight loss; what about other parameters?

In our opinion this is where the BROAD study lets itself down; it’s not that these results are terrible, but that the discussion of them, such as it is, amounts to special pleading. HDL was low (“high risk”) at baseline – 1.3 mmol/l in the intervention arm; HDL didn’t change, but the TG/HDL ratio deteriorated from 2.835 to 3.170.

“CVD Risk Assessment tools are widely used in New Zealand, and although we saw intervention WC, BMI and HbA_1c improve, the between-group CVD RA (which does not account for some of these) did not change significantly. Also, HDL-cholesterol tends to decrease on a plant-based diet, and previous research had shown this ‘may not be helpful for predicting cardiovascular risk in individuals consuming a low-fat, plant-based diet’. Our analysis corroborates that this tool is not particularly appropriate for those consuming a WFPB diet.”

Now, this may well be true, but the reference for this claim is one 30-day cohort study (no comparison arm) using the same kind of wishful thinking.[3] What would be more convincing would be a mechanistic explanation of why lower HDL levels are tolerable on a very low fat diet, maybe through the diet’s effect on HDL subtype, or HDL efflux capacity, or an interaction with very low LDL, demonstrated in feeding studies. However, LDL in the intervention arm was 3 mmol/l at 12 months which though almost within target is not especially low, and the TG/HDL ratio predicts that the percentage of small dense LDL will be relatively high, so we do need more than wishful thinking before discounting the relevance of these scores. If we were to claim that a lack of effect on LDL didn’t matter in a low carb study, we would have no shortage of mechanistic evidence from feeding studies and risk factor studies to explain why; there is a huge body of scientific investigation about lipoproteins that can be relevant to these sorts of cases.

Where the discussion goes badly wrong is in attacking LCHF diets using evidence that is thin and irrelevant. The numbers of people in LCHF trials and feeding studies has become large enough that patterns of adverse outcomes can be decided by the evidence from these studies. As prior to recent years very few people in the general population ate LCHF diets, epidemiological studies don’t give us this evidence.

So what do we get, by way of a discussion of superiority?

Reviews comparing the WFPB approach to other diets show similar weight loss at 12 months for low-carbohydrate and low-fat diet approaches. However, studies on the effects of low-carbohydrate diets have shown higher rates of all-cause mortality,⁵⁴ decreased peripheral flow-mediated dilation,⁵⁵worsening of coronary artery disease,⁵⁶ and increased rates of constipation, headache, halitosis, muscle cramps, general weakness and rash.

This isn’t good enough. Reference 54, Noto et al, is a notorious mishmash of epidemiological studies, uses an idiosyncratic and unrealistic scoring system, is mostly concerned with protein (or at least certainly conflated with it),  and includes no evidence from low carbohydrate diet trials. In fact, because more recent evidence shows that higher fat intake was associated with lower mortality in the Nurses Health Study and Health Professionals Follow up Study, and lower cardiovascular mortality in the Malmo Diet and Cancer study, not to mention the forthcoming PURE study, this line of evidence, even were it admissible, is no longer supportive of the claim. Reference 55 combines 5 studies only one of which had significant results – in any case, FMD is an insulin-mediated response to glucose in the bloodstream and its reduction, while possibly undesirable and indicative of insulin resistance on a high-carb diet, would seem to be a normal adaptation to the absence of carbohydrate. Reference 56 relates to people eating high protein during an uncontrolled low fat, high carbohydrate intervention – how high, and what else did they eat differently? It’s impossible to tell from the paper, which is a singularly inappropriate piece of evidence to use in an attack on low carb. [Edit 2019 – the investigation and retraction of a recent paper by the author of Ref 56 suggests many problems with his work. That it was included in the BROAD study despite faults obvious to us when this review was first written highlights the thinness of the body of supportive research plant-based writers are relying on].

What about “increased rates of constipation, headache, halitosis, muscle cramps, general weakness and rash”? Some of these are expected temporary effects of keto-adaptation or of insufficient salt intake during low-carb induced natriuresis. Rash can result from increased intake of unrefined plant foods in people who are salicylate-intolerant, so is a possible side effect of vegan diets too.

The greatest weakness of this paper is its failure to discuss at all two findings; firstly that blood pressure increased on the WFPB diet. This was not statistically significant (p=0.06) but as it is an underpowered trial and this result ran counter to expectations it is worth explaining; possibly a reduction in medication can account for it.

Secondly, one person in the intervention arm had their gallbladder removed due to gallstones at 5 months. This is a known adverse effect of weight loss on a very low fat diet.[4,5] It was the subject of a 2014 meta-analysis, which found that “diets high in fat content reduced gallstones, compared with those with low fat content (risk ratio, 0.09; 95% CI, 0.01-0.61)”.[6] This would seem to be more serious than the known side effects of low carb diets. Though the one event of this sort in BROAD cannot be statistically significant, the authors (and reviewers) should have been aware of similar occurrences in other trials, making this an important risk to discuss.

Adherence at 12 months was 70% but no-one’s reason for dropping out was given.
(The informed consent phase meant that people who agreed to be in the study were aware that a vegan diet would be the only diet they were likely to get. This could be seen as a different situation in terms of self-selection bias from those studies which offer an equal chance of getting a low carb diet or a calorie-restricted 30% fat diet; people who didn’t specifically want a vegan diet could opt out, knowing their care would be the same, whereas with a two-diet comparison people may be more likely to enter the study but drop out after learning what diet they have been randomised to.)

Although this study obtained very good results in terms of weight loss, a definite win for its participants, the authors’ unwillingness to discuss possible negatives and their over-eagerness to attack low carb interventions without real evidence (they should have saved their bile for the “usual medical care” that failed their patients) do not enhance this paper’s value.

Nor does the appeal to the environmental sustainability and greenhouse gas footprint, which depends on a 2014 UK modelling paper. It all depends what foods you eat – at present these models use the lean meat, low fat dairy recommendations; however, animal fat and organ meat are wasted products, adding up to a lot of energy and nutrition, of producing these that we could use a lot more wisely. A vegan diet will have a larger environmental impact if you need to eat more imported food and out-of-season (not a problem with NZ beef and lamb) and food with a higher water content, which isn’t a very economical use of land. Raising monoculture plant crops uses more fossil fuels and has a worse effect on the land than raising ruminants the way we do in New Zealand (something you might miss with a UK model, where a lot of meat is imported). It is early days for that kind of research and all we have so far is speculative models based on assumptions.

Take homes? This trial tells us little about eating meat. It shows that getting off sugar, and refined foods has a good effect on short and medium term weight loss on this intensive intervention group compared to usual care. However an effect may be the worsening of some CVD risk factors, although what this really means isn’t clear. It says nothing about low carb healthy fat eating.

References

[1] Wright N, Wilson L, Smith M, Duncan B, McHugh P. The BROAD study: A randomised controlled trial using a whole food plant-based diet in the community for obesity, ischaemic heart disease or diabetes. Nutrition & Diabetes. 2017; 7(e256) doi:10.1038/nutd.2017.3. http://www.nature.com/nutd/journal/v7/n3/full/nutd20173a.html

[2] McKenzie AL, Hallberg SJ, Creighton BC, Volk BM, Link TM, Abner MK, Glon RM, McCarter JP, Volek JS, Phinney SD
A Novel Intervention Including Individualized Nutritional Recommendations Reduces Hemoglobin A1c Level, Medication Use, and Weight in Type 2 Diabetes
JMIR Diabetes 2017;2(1):e5. DOI: 10.2196/diabetes.6981

[3] Kent L, Morton D, Rankin P, et al. The effect of a low-fat, plant-based lifestyle intervention (CHIP) on serum HDL levels and the implications for metabolic syndrome status – a cohort study. Nutrition & Metabolism. 2013;10:58. doi:10.1186/1743-7075-10-58.

[4] Festi D, Colecchia A, Orsini M, et al. Gallbladder motility and gallstone formation in obese patients following very low calorie diets. Use it (fat) to lose it (well). Int J Obes Relat Metab Disord. 1998; 22(6):592-600.

[5] Gebhard RL, Prigge WF, Ansel HJ, Schlasner L, Ketover SR, Sande D, Holtmeier K, Peterson FJ. The role of gallbladder emptying in gallstone formation during diet-induced rapid weight loss. Hepatology. 1996; 24(3):544-8.

[6] Stokes CS, Gluud LL, Casper M, Lammert F. Ursodeoxycholic acid and diets higher in fat prevent gallbladder stones during weight loss: a meta-analysis of randomized controlled trials. Clin Gastroenterol Hepatol. 2014 Jul;12(7):1090-1100.e2; quiz e61. doi: 10.1016/j.cgh.2013.11.031. Epub 2013 Dec 7.