Economic Benefits of Taxing Sugary Drinks

It is interesting reading about the tax on sugary drinks that David Mendosa wrote about here after the votes on November 8, 2016. Now we have more information from a study led by the University of East Anglia (UEA). The researchers state that the wider economic benefits of a tax on sugary drinks need to be recognized by policymakers if retailers' pricing behavior is to be changed.

The researchers argue that economic welfare would be improved if firms could be dissuaded from using 'value size' pricing - which involves deliberately selling larger size drinks at much lower unit prices than smaller sizes - and this economic benefit would be in addition to the health benefit from reduced consumption of harmful sugary drinks.

Such value size pricing is exceptionally harmful when it leads to excessive consumption of unhealthy foods and drinks, as well as exploiting consumers who wish to limit their consumption and stick to smaller sizes for their own health and enjoyment.

This makes sense if communities are taxing sugary drinks and needs to be understood by consumers.

Last month the UK government published draft legislation for a tax on sugar-sweetened drinks, which is set to begin from April 2018. The rate has yet to be set but it is hoped the move will help tackle the nation's obesity problem.

In the US, several cities are now considering introducing or reviewing their existing soda taxes. Other countries, notably France, Hungary and Mexico, have such taxes already, while South Africa, Australia and New Zealand may be contemplating introducing them.

The UEA study models how a retailer, be they a supermarket, restaurant, or any outlet selling drinks for immediate consumption, might use different sizes of sugary drinks with different relative prices to target different consumer groups. It then considers how policy measures might change the vendor's behavior and affect consumer choices.

The authors warn that policymakers should not underestimate the determination of retailers to profitably segment consumers and that poorly designed measures which do not fully take this aspect into account can damage rather than improve economic welfare.

They say their findings, published in the Journal of Business Research, provide further justification for introducing a substantial soft drinks industry levy to tackle the problem of excessive consumption of sugary drinks fueling obesity.

The study was led by Paul Dobson, Professor of Business Strategy and Public Policy at UEA's Norwich Business School, working with Ratula Chakraborty, also of Norwich Business School, and Dr Jonathan Seaton from Loughborough University. Prof Dobson said that the drinks industry is seeking to make any levy as low as possible when in fact it needs to be high in order to change pricing behavior in a meaningful way.

"Our paper conveys a really important point that is fundamental to public policy making in this area but which has been entirely overlooked," said Prof Dobson. "This is that the current basis for intervention to restrict the excessive quantity of sugary drinks rests entirely on the premise that this will be good for the health of consumers and a cost saving to society from reduced healthcare costs.

"However, there are good economic reasons as well as health reasons to have a sugary drinks tax as a means to curb excessive consumption of calorie-laden sugary drinks and encourage more efficient pricing. A soft drinks industry levy needs to be set high enough to ensure that the retailers are discouraged from imposing a surcharge on smaller drinks sizes, which penalizes moderating consumption in order to steer consumers towards consuming excessively through relative discounts and multi-buy offers on large drinks sizes."

In one recent example of the kind of temptation that value size pricing offers consumers, a leading supermarket retailer selling a sugary carbonated drink was offering the following prices before Christmas: buy two 1.75 liter bottles for £2 (1470 kcal at 2.3 pence per teaspoon of sugar), one 1.75 liter bottle for £1.66 (735 kcal at 3.8 pence per teaspoon of sugar) or one 0.5 liter bottle for £1.25 (210 kcal at 9.9 pence per teaspoon of sugar). The unit price of the latter small size bottle was more than four times higher than on the multi-buy offer on the large size bottle.

Similar incentives to 'go large' exist at restaurants, fast-food outlets and other eateries where for a few extra pence or cents consumers can supersize their sugary drinks or have free refills.

Prof Dobson said: "It is no wonder that many consumers feel compelled to take advantage of the size discount and then consequently over consume. Equally, those consumers sticking to the small size can feel aggrieved at being penalized by paying a high price for their discipline in restricting their consumption.

"It is the exploitation of these disciplined consumers which puts off other consumers from restricting their purchase sizes in favor of the temptation of grabbing a supposed bargain because of the way the offer is couched as a 'discount', when in fact it is the small size which suffers a 'surcharge' from which the retailer can handsomely profit.

"Policy measures which dissuade retailers from using such pricing tactics to drive higher volumes of sugary drinks are therefore justified on both health and economic grounds."

Diagnosing Diabetes and Prediabetes

The following tests are used for the diagnosis of diabetes:

1. A fasting plasma glucose test (FPG) measures your blood glucose after you have gone at least 8 hours without eating. This test is used to detect diabetes or prediabetes.
2. An oral glucose tolerance test (OGTT) measures your blood sugar after you have gone at least eight hours without eating and two hours after you drink a glucose-containing beverage. This test can be used to diagnose diabetes or prediabetes.
3. In a random plasma glucose test (PGT), your doctor checks your blood sugar without regard to when you ate your last meal. This test, along with an assessment of symptoms, is used to diagnose diabetes, but not prediabetes.
4. Newer guidelines use hemoglobin A1c (HbA1c) as a screening tool for prediabetes or diabetes (the test is normally used to measure blood glucose control in diabetes patients over several months). An HbA1c of 5.7% to 6.4% is consistent with prediabetes and marks a time when it can be reversed by lifestyle changes. An HbA1c of 6.5% or higher is consistent with diabetes. Normally, this test is repeated for confirmation.

Positive test results should be confirmed by repeating the fasting plasma glucose test or the oral glucose tolerance test on a different day. When first diagnosed with diabetes, your doctor may suggest a zinc transporter autoantibody (ZnT8Ab) test. This blood test -- along with other information and test results -- can help determine if a person has type 1 diabetes and not another type. The goal of having the ZnT8Ab test is a prompt and accurate diagnosis and that can lead to timely treatment.

The FPG is most reliable when done in the morning. Results and their meaning are shown in table 1. If your fasting glucose level is 100 to 125 mg/dl, you have a form of prediabetes called impaired fasting glucose (IFG), meaning that you are more likely to develop type 2 diabetes but do not have it yet. A level of 126 mg/dl or above, confirmed by repeating the test on another day, means that you have diabetes.

Table 1. Fasting Plasma Glucose Test

Plasma Glucose Result (mg/dl)	Diagnosis
99 and below	Normal
100 to 125	Prediabetes (impaired fasting glucose)
126 and above	Diabetes*

*Confirmed by repeating the test on a different day.

Research has shown that the OGTT is more sensitive than the FPG test for diagnosing prediabetes, but it is less convenient to administer. The OGTT requires you to fast for at least eight hours before the test. Your plasma glucose is measured immediately before and two hours after you drink a liquid containing 75 grams of glucose dissolved in water. Results and what they mean are shown in table 2. If your blood sugar level is between 140 and 199 mg/dl 2 hours after drinking the liquid, you have a form of prediabetes called impaired glucose tolerance or IGT, meaning that you are more likely to develop type 2 diabetes but do not have it yet. A two-hour glucose level of 200 mg/dl or above, confirmed by repeating the test on another day, means that you have diabetes.

Table 2. Oral Glucose Tolerance Test

2-Hour Plasma Glucose Result (mg/dl)	Diagnosis
139 and below	Normal
140 to 199	Prediabetes (impaired glucose tolerance)
200 and above	Diabetes*

*Confirmed by repeating the test on a different day.

Gestational diabetes is also diagnosed based on plasma glucose values measured during the OGTT. Blood sugar levels are checked four times during the test. If your blood sugar levels are above normal at least twice during the test, you have gestational diabetes. Table 3 shows the above-normal results for the OGTT for gestational diabetes.

Table 3. Gestational Diabetes: Above-Normal Results for the Oral Glucose Tolerance Test

When	Plasma Glucose Result (mg/dl)
Fasting	95 or higher
At 1 hour	180 or higher
At 2 hours	155 or higher
At 3 hours	140 or higher

Note: Some laboratories use other numbers for this test.

For additional information about the diagnosis and treatment of gestational diabetes, see the NIDDK booklet What I Need to Know about Gestational Diabetes.

A random blood glucose level of 200 mg/dl or more, plus presence of the following symptoms, can mean that you have diabetes:

• Increased urination
• Increased thirst
• Unexplained weight loss

Other symptoms include fatigue, blurred vision, increased hunger, and sores that do not heal. Your doctor will check your blood glucose level on another day using the FPG, OGTT, and the HbA1c to confirm the diagnosis of diabetes.

Possible Ways to Improve Artery Repair

Research may point towards more effective surgical stents for people with diabetes. People with any form of diabetes are at greater risk of developing cardiovascular conditions than people without the disease. Moreover, if they undergo an operation to open up a clogged artery by inserting a "stent" surgical tube, the artery is much more likely to clog up again. However, researchers at Joslin Diabetes Centers now have uncovered an explanation for why these procedures often fail, which may lead toward better alternatives.

An enzyme known as SHP-1, which can suppress the growth of smooth muscle cells lining the inside of blood vessels, plays a crucial role in stent failure, says George King, M.D., Joslin's Chief Scientific Officer and senior author on a paper in the journal Diabetologia describing the work.

Stents coated with a drug that activates SHP-1, and thus slows the accelerated growth of these vascular cells, might help in treating arterial disease in diabetes, says King, who is also Professor of Medicine at Harvard Medical School.

His team's research began with experiments among mice fed a high-fat diet and rats that were genetically modified to display insulin resistance and related metabolic conditions related to diabetes. "We found that SHP-1 expression was decreased in the arteries from all of these animal models," says Weier (Glorian) Qi, co-lead author on the paper. "We also found that SHP-1 expression dropped in the arteries of patients with type 2 diabetes."

Next, the scientists created mice that were genetically engineered to over-express the protein in their vascular smooth muscle cells. When the scientists fed these mice a high-fat diet that clogged their arteries and performed a procedure similar to stent insertion, they found that the arteries in these animals were less clogged than in normal mice given the same procedure.

The researchers went on to demonstrate that SHP-1 is reduced in mouse vascular smooth muscle cells primarily by the high levels of lipids in the blood associated with diabetes and related conditions, rather than the high levels of glucose also present in those conditions.

Following up on these findings may help to address a major research puzzle in diabetic complications, says King: Each type of tissue seems to react differently to the disease.

For example, he explains, smooth muscle cells grow thicker in large blood vessels like arteries, but similar type of contractile cells begin to die off in tiny blood vessels in the eye.

"These opposite cell growth patterns are an enigma," King comments. "They also make it difficult to develop therapeutics, because we would want to deactivate SHP-1 in the eye and activate it in large arteries."

Surgical stents for artery repair are typically coated with slow-releasing drugs that aim to suppress excessive regrowth of the surrounding smooth muscle cells. This approach to release drugs locally might work for drugs that boost SHP-1 expression, King speculates.

"We hope our research encourages ideas about how to address this problem for people with diabetes," he adds. ""The more ideas that come up, the greater the chances that we can achieve such a needed treatment."

This is one reason that I am hesitant to follow the high fat part of the low carb high fat diet, although I do use the low carb medium fat and moderate protein of my own choosing.

Vitamin K and D Have a Relationship

Vitamin K describes a family of compounds with a common chemical structure. These compounds include vitamin K1 (phylloquinone) and multiple forms of vitamin K2 (menoquinones/MK), all of which are fat soluble.

Vitamin K primarily functions as a coenzyme, a protein that speeds up a reaction, for the synthesis of proteins involved in blood clotting and bone metabolism. Prothrombin is a vitamin K dependent protein vital for blood coagulation. This explains why patients on anticoagulants, such as Warfarin, must avoid vitamin K supplementation.

Osteocalcin is also a vitamin K dependent protein that plays a role in bone building and mineralization. Although, little is known about vitamin K’s function in bone.

In recent years, researchers have taken an interest in a matrix Gla-protein (MGP), yet another vitamin K dependent protein, present in blood vessel walls, bone and cartilage. Researchers have found that MGP may help reduce abnormal calcification.

Traditionally, vitamin D has been known for its role in bone health, allowing for proper bone mineralization to occur. However, in the past decade, researchers have discovered that maintaining healthy vitamin D levels provides a myriad of benefits for human health, ranging from reducing one’s risk of cancer to aiding in the treatment of multiple sclerosis. These profound effects are primarily attributed to vitamin D’s combination of anti-inflammatory and anti-microbial properties.

Vitamin D toxicity poses a risk to one’s health when supplementing with very large doses, such as 40,000 IU of vitamin D daily. Toxicity results from excessively high calcium levels, known as hypercalcemia.

To maximize the benefits of vitamin D supplementation while also minimizing the potential risk of toxicity, some experts believe that vitamin K supplements should be taken adjunctively to vitamin D. As mentioned previously, vitamin K activates the MGP, a protein that helps direct calcium to the desirable places (bone) and lead calcium away from the undesirable places (arteries). Thus, one would expect the risk of hypercalcemia to decrease when supplementing with vitamin K.

A longitudinal study published in September 2016 assessed the vitamin D levels and uncarboxylated matrix Gla-protein levels (MGP) of 257 men and women between the ages of 55-65 who were free of cardiovascular disease and hypertension. The uncarboxylated MGP levels indicate the lack of vitamin K, because the MGP becomes carboxylated from vitamin K. Thus, a high level of uncarboxylated MGP represents a low level of vitamin K.

The researchers followed the participants’ health for six years. Over this time, approximately half of the cohort developed hypertension. The researchers determined that both low vitamin D and high uncarboxylated MGP levels were associated with an increased risk for developing hypertension (HR: 1.72) after adjusting for age, body mass index and type II diabetes. The risk of developing hypertension was much more profound with both low vitamin D and high uncarboxylated MGP levels compared to the risk with solely low vitamin D levels or solely high uncarboxylated MGP levels (HR 1.08 and 1.43, respectively).

Since both vitamin D and vitamin K play a role in bone mineralization, researchers conducted a study to see if low vitamin K1 and vitamin D levels were associated with an increased risk of hip fracture among the elderly population in Oslo, Norway. The researchers compared the vitamin D levels of 111 hip fracture patients and 73 healthy participants.

The study concluded that low vitamin K1 and vitamin D levels are independently and synergistically associated with an increased risk of hip fractures after adjusting for confounding factors.

In 2015, researchers conducted a RCT with 42 non-dialysis CKD patients. Twenty nine patients were randomly assigned to receive a daily oral dose of 90 μg of vitamin K2 plus 400 IU of vitamin D per day for about 270 days. The remaining thirteen patients were assigned to receive 400 IU of vitamin D.

The researchers discovered that vitamin K supplementation in conjunction to vitamin D supplementation reduced the progression of atherosclerosis in patients with chronic kidney disease (CKD) significantly more so than supplementing with vitamin D alone.

Oxidative stress results from an imbalance of free radicals and antioxidants. Free radicals inflict damage to DNA; whereas antioxidants protect against free radicals. Oxidative stress is thought to be involved in the development of various diseases and conditions, such as cancer, Alzheimer’s disease, atherosclerosis, autism and chronic fatigue.

A randomized controlled trial published in July 2016 assessed the effects of vitamin D, vitamin K and calcium co supplementation among 60 vitamin D deficient women with Polycystic Ovary Syndrome (PCOS), a common condition in which a woman experiences hormonal imbalances. The researchers assessed hormone levels, oxidative stress, antioxidant levels, among other outcomes.

They found that 8 weeks of supplementation with 200 IU vitamin D, 90 μg vitamin K and 500 mg of calcium twice a day resulted in a significant decrease of serum-free testosterone, while total antioxidant capacity and oxidative stress significantly increased compared to the placebo group.

The study did not possess enough study groups to determine whether the beneficial effects were attributed to one vitamin/mineral, or the combination of taking all. However, the improvement of oxidative stress and anti-oxidant levels warrants further research.

Research indicates that vitamin D and vitamin K work synergistically to optimize one’s health, especially concerning bone and heart health. Thus, it is important to take the proper steps to ensure that you are maintaining healthy levels of both vitamin K and vitamin D.

Unlike most vitamins and minerals, vitamin D cannot be found in adequate amounts from dietary sources. We must rely on either safe, sensible sun exposure or supplementation on a daily basis to ensure vitamin D sufficiency. The Vitamin D Council recommends supplementing with 5000 IU of vitamin D3 daily on days that you cannot get adequate sun to achieve a status between 40-60 ng/ml. After two months of supplementation, it is important to  measure your vitamin D levels and adjust your supplementation regimen accordingly.

On the other hand, vitamin K can be found in the following foods:

• Vitamin K1: green leafy vegetables
• Vitamin K2: hard cheeses, such as gouda or brie, Natto (Japanese fermented soybeans) and organ meats

In addition, the human gut produces vitamin K2.

Therefore, while reviewing the foods that contain vitamin K and the amount that you need, you can approximate whether you receive adequate vitamin K from your diet. If you do not, the Vitamin D Council recommends increasing your intake of the dietary sources listed above or begin supplementing.

Biotech’s Vitamin D3 Plus offers a perfect option to those who want to ensure they maintain adequate vitamin D levels while also receiving vitamin D’s cofactors.

PCSK9 Inhibitors Increase Diabetes Risk

I think Dr. Malcolm Kendrick will be happy to see this study. Back in July 2015, he predicted this would happen. The results of two independent studies of genetic variants suggest that treatment with a PCSK9 inhibitor could increase the riskfor diabetes.

In the first study, involving 112,772 participants, the researchers constructed two genetic scores consisting of PCSK9 and HMGCR variants to mimic the effects of treatment with PCSK9 inhibitors and statins, respectively. They found that low-density lipoprotein (LDL) cholesterol-lowering variants in both genes were associated with a reduction in the risk for cardiovascular events, but an elevated risk for diabetes.

After adjustment for a decrease in LDL cholesterol levels of 10 mg/dl, the team found a “nearly identical” reduction of 18.9% and 19.1% in the risk for cardiovascular events with the presence of PCSK9 and HMGCR variants, respectively.

These findings suggest that “treatment with a PCSK9 inhibitor should reduce the risk of cardiovascular events by approximately the same amount as treatment with a statin,” write study authors Brian Ference (Wayne State University School of Medicine, Detroit, Michigan, USA) and colleagues in The New England Journal of Medicine.

However, the presence of PCSK9 variants was associated with an 11.2% increase in the risk for diabetes per decrease of 10 mg/dl in LDL cholesterol, and the presence of HMGCR variants was associated with a 12.7% increase in risk.

“Like statins, PCSK9 inhibitors may also increase the risk of new-onset diabetes,” say the authors. However, because the proportional reduction in cardiovascular disease risk associated with PCSK9 variants was “much greater” than the increased risk for diabetes, they conclude that “as with statins, the reduction in cardiovascular risk with PCSK9 inhibitors should far exceed any potential increased risk of diabetes.”

In the second study, Amand Schmidt (University College London, UK) and colleagues analyzed data from 568,448 individuals included in randomized controlled trials, observational studies, and genetic consortia to estimate the association between PCSK9 variants and type 2 diabetes risk.

The team showed that four independent PCSK9 variants were associated with a reduction in LDL cholesterol levels, ranging from 0.02 mmol/L (0.78 mg/dl) to 0.34 mmol/L (13.15 mg/dl) per LDL cholesterol-reducing allele.

When the variants were combined into a weighted gene-centric score and scaled to a reduction in LDL cholesterol of 1 mmol/L (38.67 mg/dl), presence of the variants was associated with a 29% increased risk for type 2 diabetes.

The study authors also found that PCSK9 variants were associated with increased fasting glucose, body weight, and waist-to-hip ratio, but not with glycated hemoglobin, fasting insulin, or body mass index.

"Genetic variants in PCSK9 that associate with lower concentrations of LDL cholesterol are also associated with a modestly higher risk of type 2 diabetes and with associated differences in measures of glycemia,” write the authors in The Lancet Diabetes and Endocrinology.

They recommend that future trials of PCSK9 inhibitors should carefully monitor changes in metabolic markers, including body weight and glycemia, and conclude that genetic studies “could be more widely used to interrogate the safety and efficacy of novel drug targets.”

Brain Atrophy Prevented By Mediterranean Diet

Since I don't follow the Mediterranean diet, I am presenting this as is and with some doubts. They say that mounting evidence emphasizes the health benefits of a Mediterranean diet. New research suggests the healthful diet helps to preserve brain volume in elderly adults.

Increasingly studies seem to suggest that components of the Mediterranean diet, either in isolation or taken together, can have a beneficial effect on various aspects of human health.

The "traditional" Mediterranean diet - consisting of large amounts of fruits and vegetables, whole grains, olive oil, a moderate amount of fish, dairy, and wine, as well as a limited intake of red meat - has been shown to improve cardiometabolic health.

Research ranging from observational studies to randomized trials has shown the diet to reduce the risk of type 2 diabetes and obesity, aid weight loss, and contribute to the prevention of cardiovascular disease.

Other studies have suggested that the diet helps to keep mental and physical health well into old age and can reduce the risk of premature death.

New research published in Neurology, the medical journal of the American Academy of Neurology, looks specifically at the benefits of the Mediterranean diet on brain health in elderly adults.

Researchers led by Michelle Luciano, Ph.D. - from the University of Edinburgh in Scotland - looked at the effects of the Mediterranean diet (MeDi) on total brain volume, gray matter volume, and the thickness of the cortex.

The authors explain that, with age, the human brain shrinks, and more and more of its cells die. This may cause problems with learning and memory.

The study followed 967 people aged between 73 and 76 years, who lived in Scotland and who did not have dementia, over a period of 3 years.

The 967 participants were asked to complete food questionnaires when they were 70 years old - 3 years prior to collecting data on their brain volume. Then, 562 of these people had a magnetic resonance imaging brain scan at the age of 73, in order to measure total brain volume, gray matter volume, and cortical thickness. Of these, 401 people had a second brain scan at age 76.

People's dietary habits were calculated using a food frequency questionnaire. The brain measurements were compared with how well the participants adhered to the MeDi during the 3-year period. The scientists found an association between MeDi adherence and brain volume.

Participants who did not follow the diet closely were likely to develop brain atrophy over the 3-year interval.

More specifically, poor adherence to the diet was associated with a 0.5 percent greater reduction in total brain volume than those who had followed the diet closely. A 0.5 percent decrease in brain volume is half the size of what is considered a normal decrease due to the natural aging process.

Researchers adjusted for variables that might have influenced the changes in brain volume, including age, education, and health conditions such as diabetes or hypertension. The study found no association between the diet and gray matter volume or thickness of the cortex.

Contrary to previous studies, this research did not find a relationship between fish and meat consumption and changes in brain volume. This suggests that other individual components of the diet - or all of its components taken in combination - might be responsible for the association.

Additionally, unlike previous research - which measured the brain at one point in time - this study examined changes in brain volume over time. "In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain. Still, larger studies are needed to confirm these results."

Dietitians Are Harming Themselves

Yes, dietitians around the world are harming themselves. First, they are not all an example of health, with many of them being overweight and a few are very obese. I have heard from many people that will not follow what the overweight or obese dietitians recommend. This obviously is something that harms them and means that people don't believe what they say.

Here in the United States, we have other problems of dual titled CDEs and RDs that refuse to teach about diabetes and seem to always switch to nutrition as being the most important. At least we have our members and several of the other support groups calling the insurance company when this happens and the recommendation for diabetes education only. This prevents the dual titled from billing for diabetes education when they taught only nutrition.

The following are blogs for your reading:

Blogs from Low Carb Diabetic.

http://thelowcarbdiabetic.blogspot.com/2017/01/evidence-that-supports-prescription-of.html

http://thelowcarbdiabetic.blogspot.com/2017/01/would-you-take-flying-lessons-from.html

http://thelowcarbdiabetic.blogspot.com/2017/01/are-dietitians-selling-us-out.html

http://thelowcarbdiabetic.blogspot.com/2017/01/behaviour-of-low-carb-antis-explained.html

http://thelowcarbdiabetic.blogspot.com/2017/01/low-carbers-can-never-lose-here-is-why.html

http://thelowcarbdiabetic.blogspot.com/2017/01/the-british-dietetic-associations-role.html

http://thelowcarbdiabetic.blogspot.com/2016/12/type-2-diabetic-heres-real-dietitian.html

http://thelowcarbdiabetic.blogspot.com/2016/12/no-xmas-card-from-drcarrie-ruxton-rd.html

http://thelowcarbdiabetic.blogspot.com/2016/12/politicians-bda-dietitians-and-other.html

http://thelowcarbdiabetic.blogspot.com/2016/11/the-british-dietetic-association-cyber.html

Blogs from me.

http://bobsdiabetes.blogspot.com/2017/01/dietitians-role-in-diabetes-and-obesity.html

http://bobsdiabetes.blogspot.com/2016/12/dietitians-being-called-out-by-bloggers.html

http://bobsdiabetes.blogspot.com/2016/12/dietitian-controversy.html

http://bobsdiabetes.blogspot.com/2016/12/dietetic-associations-around-world-are.html

http://bobsdiabetes.blogspot.com/2016/11/anarchy-exists-where-dietitians-rule.html

http://bobsdiabetes.blogspot.com/2016/10/coca-cola-pepsico-funded-health.html

http://bobsdiabetes.blogspot.com/2016/10/dietitians-and-their-lies.html

http://bobsdiabetes.blogspot.com/2016/03/lchf-being-discouraged-by-dietitians.html

If you have already read my blogs, good, but I hope that you will read the others as they describe what is happening in Great Britain and other parts of the world.