When the Dietitians Association of Australia (DAA) isn’t dishing up fake nutrition news to the public, it makes up fake news to try to discredit dietitians who cross it, say critics. It’s probably no coincidence, that those dietitians support low-carb, high-fat (LCHF) diets to treat obesity, diabetes and heart disease and/or criticise Australia’s dietary guidelines and DAA’s food industry links.
Critics say that DAA’s Big Food sponsors don’t like those dietitians either as they affect product sales. In the final of a four-part series on DAA’s conflicts of interest, Foodmed.net looks at the cases of three dietitians who fell foul of DAA and its long-time CEO Claire Hewat. DAA also thought nothing of going after one of the dietitians in another country. It tried and failed to silence a top dietitian academic in New Zealand for her views on LCHF.
Hewat flatly denies that LCHF or its industry links had anything to do with actions against the dietitians below. Here, Foodmed.net looks at whether that claim stands up to scrutiny.
Virtually all doctors agree that elevated insulin resistance is very bad for human health, being the root cause of type 2 diabetes and metabolic syndrome. So, if it is so bad, why do we all develop it in the first place? How can such a mal-adaptive process be so ubiquitous?
As of 2015, over 50% of the American population has diabetes or pre-diabetes. This stunning statistic means that there are more people in the United States with pre-diabetes or diabetes than without it. It’s the new normal. Why does it develop it so frequently? There must be some protective purpose to it since our bodies are not designed to fail. Humans have lived for millennia before the modern diabesity epidemic. How can insulin resistance be protective?
You can discover many things by taking a different perspective. The golden rule states “Do unto others as you would have them do unto you.” A well-known quote says, “Before you judge me, walk a mile in my shoes”. In both cases, the key to success is change perspective. Invert (turn upside down) your perspective, and see how your horizons are immensely broadened. So let’s look at the development of insulin resistance from the opposite angle. Let’s not consider why insulin resistance is bad, but rather, why it is good.
Over the past half-century, the rate of obesity in America has nearly tripled, while the incidence of diabetes has increased roughly seven-fold. It’s estimated that the direct health care costs related to obesity and diabetes in the United States is $1 billion a day, while economists have calculated the indirect costs to society of these epidemics at over $1 trillion a year.
In recent years, some researchers have focused on the particular role refined sugar may play in these epidemics. Perhaps the most comprehensive analysis of this research has been put forth by the science journalist, Gary Taubes, author of the recent book, “The Case Against Sugar.” I spoke with Taubes about his research and what people should know about sugar to make better choices in their diets.
David Bornstein: What’s the essence of the case against sugar?
Gary Taubes: To understand the case against sugar, using a criminal justice metaphor, you have to understand the crimes committed: epidemics of diabetes and obesity worldwide. Wherever and whenever a population transitions from its traditional diet to a Western diet and lifestyle, we see dramatic increases in obesity, and diabetes goes from being a relatively rare disorder to a common one. One in 11 Americans now has diabetes. In some populations, one in three or four adults have diabetes. Stunning numbers.
So why sugar? Well, for starters, recent increases in sugar consumption are always at the scene of the crime on a population-wide level when these epidemics occur. And sugar is also at the scene of the crime biologically, and it’s got the mechanism necessary. But the evidence is not definitive; what I’m arguing is still a minority viewpoint.
Starchy foods are the main sources of carbohydrates; however, there is limited information on their metabolic impact. Therefore, we assessed the association between carbohydrates from starchy foods (Carb-S) intakes and the metabolic disorders of metabolic syndrome (MetS) and hyperlipidemia. In this study, 4,154 participants from Northern China were followed up for 4.2 years. Carb-S included rice, refined wheat, tubers, and their products. Multivariable regression models were used to calculate risk ratios (RRs) for MetS and hyperlipidemia from Carb-S, total carbohydrates, and carbohydrates from other food sources (Carb-O). Receiver operating characteristic analysis was used to determine a Carb-S cut-off value. High total carbohydrate intake was associated with increased risks of MetS (RR: 2.24, 95% CI: 1.00–5.03) and hyperlipidemia (RR: 3.05, 95% CI: 1.25–7.45), compared with the first quartile. High Carb-S intake (fourth quartile) was significantly associated with MetS (RR: 1.48, 95% CI: 1.01–2.69) and hyperlipidemia (RR: 1.73, 95% CI: 1.05–3.35). No associations with Carb-O were observed. Visceral adiposity, triglyceride levels, and high-density lipoprotein cholesterol significantly contributed to the metabolic disorders. The Carb-S cut-off value was 220 g. Both high total carbohydrate and Carb-S intakes were associated with hyperlipidemia and MetS; Carb-S appears to contribute more to these disorders.
When their father, Geoff, was diagnosed with type 2 diabetes at the age of 50, brothers Ian and Anthony Whitington were not hugely surprised, and for 10 years, they drifted along and watched from the sidelines.
“Dad had always been the ‘big man’,” says Anthony, 39. “As kids, we thought it was funny. Dad could drink more than anyone, he could eat more than anyone. It was his identity. That’s our dad and that’s what he does.”
“As we got older, of course we worried,” adds Ian, 37. “But everyone around us would say, ‘If he doesn’t want to change, you can’t change him. He has to do it himself.’” So nothing much was done – and Geoff joined the 3.5m adults in the UK who manage their diabetes with ever-greater doses of medication and regular check-ups.
“We were all resigned to our family roles,” says Anthony. “I was a busy financial adviser with four kids of my own. Ian was a busy cameraman with jobs all over the world. Dad was a funny fat guy who drank too much.”
I was writing another blog, on another matter, when someone sent me an email containing a petition signed by over two hundred Canadian doctors.
Re: Canada’s Food Guide Consultation
From: Group of concerned Canadian Physicians and Allied Health Care providers
For the past 35+ years, Canadians have been urged to follow the Canadian Dietary Guidelines. During this time, there has been a sharp increase in nutrition-related diseases, particularly obesity and diabetes.
We are especially concerned with the dramatic increase in the rates of childhood obesity and diabetes. In 1980, 15% of Canadian school-aged children were overweight or obese. Remarkably, this number more than doubled to 31% in 2011; 12% of children met the criteria for obesity in the same reporting period. This has resulted in a population with a high burden of disease, causing both individual suffering, and resulting in health care systems which are approaching their financial breaking points. The guidelines have not been based on the best and most current science, and significant change is needed.
What exactly is insulin resistance? One of insulin’s jobs is to help move glucose from the blood into the cells for energy. When blood glucose remains elevated despite normal or high levels of insulin, this is called insulin resistance. The cells are resisting insulin’s pleas to take up glucose. But why is this happening? What causes insulin resistance?
The current paradigm of understanding insulin resistance is the ‘lock and key’ model. The hormone insulin acts upon a cell surface receptor to do its job. The insulin receptor is like a lock keeping the gates to the cell closed. Insulin is like the proper key. When inserted, the gate opens to let glucose from the blood inside the cell for energy. Once you remove the key (insulin), the gate closes back up and blood glucose can no longer enter the cell.
During the phenomenon of insulin resistance, we imagine that the lock and key no longer fit together very well. The key (insulin) only partially opens the lock (receptor) and not very easily. Glucose cannot pass through the gate normally, and as a result, less gets into the cell. The blood glucose piles up outside the gate, becoming detectable as the clinical diagnosis of type 2 diabetes is made.