Warning: this is a sciencey post
According to Roy Taylor, M.D., “type 2 diabetes is a potentially reversible metabolic state precipitated by the single cause of chronic excess intraorgan fat.” The organs accumulating fat are the pancreas and liver. He is certain “…that the disease process can be halted with restoration of normal carbohydrate and fat metabolism.” I read Taylor’s article published last year in Diabetes Care.
(Do you remember that report in 2011 touting cure of T2 diabetes with a very low calorie diet? Taylor was the leader. The study involved only 11 patients, eating 600 calories a day for eight weeks.)
Dr. Taylor says that severe calorie restriction is similar to the effect of bariatric surgery in curing or controlling diabetes. Within a week of either intervention, liver fat content is greatly reduced, liver insulin sensitivity returns, and fasting blood sugar levels can return to normal. During the first eight weeks after intervention, pancreatic fat content falls, with associated steadily increasing rates of insulin secretion by the pancreas beta cells.
Band Gastric Bypass Surgery (not the only type of gastric bypass): very successful at “curing” T2 diabetes if you survive the operation
Taylor’s ideas, by the way, dovetail with Roger Unger’s 2008 lipocentric theory of diabetes. Click for more ideas on the cause of T2 diabetes.
Here are some scattered points from Taylors article. He backs up most of them with references:
- In T2 diabetes, improvement in fasting blood sugar reflects improved liver insulin sensitivity more than muscle insulin sensitivity.
- The more fat accumulation in the liver, the less it is sensitive to insulin. If a T2 is treated with insulin, the required insulin dose is positively linked to how much fat is in the liver.
- In a T2 who starts insulin injections, liver fat stores tend to decrease. That’s because of suppression of the body’s own insulin delivery from the pancreas to the liver via the portal vein.
- Whether obese or not, those with higher circulating insulin levels “…have markedly increased rates of hepatic de novo lipogenesis.” That means their livers are making fat. That fat (triglycerides or triacylglycerol) will be either burned in the liver for energy (oxidized), pushed into the blood stream for use elsewhere, or stored in the liver. Fatty acids are components of triglycerides. Excessive fatty acid intermediaries in liver cells—diglycerides and ceramide—are thought to interfere with insulin’s action, i.e., contribute to insulin resistance in the liver.
- “Fasting plasma glucose concentration depends entirely on the fasting rate of hepatic [liver] glucose production and, hence, on its sensitivity to suppression by insulin.”
- Physical activity, low-calorie diets, and thiazolidinediones reduce the pancreas’ insulin output and reduce liver fat levels.
- Most T2 diabetics have above-average liver fat content. MRI scans are more accurate than ultrasound for finding it.
- T2 diabetics have on average only half of the pancreas beta cell mass of non-diabetics. As the years pass, more beta cells are lost. Is the a way to preserve these insulin-producing cells, or to increase their numbers? “…it is conceivable that removal of adverse factors could result in restoration of normal beta cell number, even late in the disease.”
- “Chronic exposure of [pancreatic] beta cells to triacylglycerol [triglycerides] or fatty acids…decreases beta cell capacity to respond to an acute increase in glucose levels.” In test tubes, fatty acids inhibit formation of new beta cells, an effect enhanced by increased glucose concentration.
- There’s a fair amount of overlap in pancreas fat content comparing T2 diabetics and non-diabetics. It may be that people with T2 diabetes are somehow more susceptible to adverse effects of the fat via genetic and epigenetic factors.
- “If a person has type 2 diabetes, there is more fat in the liver and pancreas than he or she can cope with.”
- Here’s Dr. Taylor’s Twin Cycle Hypothesis of Etiology of Type 2 Diabetes: “The accumulation of fat in liver and secondarily in the pancreas will lead to self-reinforcing cycles that interact to bring about type 2 diabetes. Fatty liver leads to impaired fasting glucose metabolism and increases export of VLDL triacylglcerol [triglycerides], which increases fat delivery to all tissues, including the [pancreas] islets. The liver and pancreas cycles drive onward after diagnosis with steadily decreasing beta cell function. However, of note, observations of the reversal of type 2 diabetes confirm that if the primary influence of positive calorie balance is removed, the the processes are reversible.”
Figure 6 from the article: Dr. Taylor’s Twin Cycle Hypothesis of Etiology of Type 2 Diabetes
- The caption with Figure 6 states: “During long-term intake of more calories than are expended each day, any excess carbohydrate must undergo de novo lipogenesis [creation of fat], which particularly promotes fat accumulation in the liver.”
- “The extent of weight gloss required to reverse type 2 diabetes is much greater than conventionally advised.” We’re looking at around 15 kg (33 lb) or 20% of body weight, assuming the patient is obese to start. “The initial major loss of body weight demands a substantial reduction in energy intake. After weight loss, steady weight is most effectively achieved by a combination of dietary restriction and physical activity.”
Dr. Taylor doesn’t specify how much calorie restriction he recommends, but reading between the lines, I think he likes his 600 cals/day for eight weeks program. That will have a have a high drop-out rate. I suspect a variety of existing ketogenic diets may be just as successful and more realistic, even if it takes more than eight weeks. I wonder how many of the 11 “cures” from the 2011 study have persisted.
Reference: Taylor, Roy. Type 2 diabetes: Etiology and reversibility. Diabetes Care, April 2013, vol. 36, no. 4, pp:1047-1055.
Update: Some wild and crazy guys tried the Taylor method at home. Click for results.
Paleo Diabetic 
Thanks so much for this post, Steve. Although caloric restriction certainly results in weight loss and other benefits, 600 calories over an eight-week period (actually, even for one week) is a starvation diet. In addition to experiencing hunger, irritability, and a reduction in resting metabolic rate, people who try such a diet will lose lean muscle as a result of inadequate caloric intake. I’d definitely argue for a ketogenic approach instead, which research suggests may preserve muscle mass during weight loss, in addition to reducing appetite and being sustainable long term. It’s also a highly palatable, luxurious way of eating that appears to have benefits beyond diabetes control and weight loss. I’ve been following a ketogenic diet containing no more than 35 grams of carbs daily for over a year and plan to continue eating this way indefinitely.
Excellent points, Franziska.
The Taylor protocol for some reason makes me think of “protein-sparing modified fasts” that were somewhat prominent in the bariatric literature about 20 years ago. That’s way before your time. IIRC, they had to be very carefully designed, supplemented, and closely medically supervised. Drop-out rates were high, as were adverse effects such as rashes and alopecia.
-Steve
Thanks, Steve.
Actually, protein-sparing modified fasts were definitely not before my time, but thanks for the compliment 🙂 It’s true that they were supplemented and medically supervised, but even at high protein levels, such severe calorie restriction results in muscle mass loss. I remember the dropout rates being very high and people suffering complications like the ones you described.
Click to access mr_119.pdf
Ma-Pi 2 Macrobiotic Diet Intervention in Adults with Type 2 Diabetes Mellitus
The group consisted of 16 adults: 3 men (18.8%) and 13 women (81.3%), average age 60 years (range: 44–73 years) and 9–31 years disease evolution. All were being treated with insulin (670 units/day total; average per capita: 42.4 units/day; 0.61 units/kg body weight) and 2 patients also used glibenclamide (6 tablets/day total; 0.2 mg/kg body weight)
At termination of the intervention, insulin administration had been eliminated in all patients, and 12 patients (75.0%) were receiving the Ma-Pi 2 macrobiotic diet as their only therapy. Overall glibenclamide use increased from 6 to 15 tablets daily (0.76 mg/kg weight), since 4 patients initiated glibenclamide therapy when they stopped taking insulin.
SO – all of the subjects came off insulin!!
Click to access JNUME2012-856342.pdf
Medium- and Short-Term Interventions with Ma-Pi 2 Macrobiotic Diet in Type 2 Diabetic Adults of Bauta, Havana
Daily diabetic medication consumption was high at onset: 53 patients used a total of 1341 insulin units (mean consumption: 25u/person and 0.3u/kgWt); 60 patients consumed 200 hypoglycemic pills (mean consumption 4tabs/person)
Consumption of Medications.
After 21 days, the mean insulin consumption dropped by 46% (617 units); 3 months later up to 858 units (64%) in relation to onset. The con- sumption of hypoglycemic pills did not show changes during the first 21 days, while 3 months later it had diminished in 10 pills (17%)
http://arab-board.org/sites/default/files/Vol.11%20No.4.pdf#page=8
THERAPEUTIC EFFECT OF MACROBIOTIC MA-PI DIET IN TYPE 1 DIABETIC CHILDREN
Dr. Parker – what are your thoughts/comments on these studies.
Hi, Charles. Thanks for sharing those links for other readers here. I don’t have time to read them, however. So best not to comment and let them speak for themselves. I vaguely recall “macrobiotics” being popular with the hippies in 1970s.
-Steve
Maybe you should read them OR do you not want to because it goes against your paradigm
I agree I should read them, it’s just a matter of finding the time. Full-time job, family life, play time, etc. When I really dig into an single journal article and blog about it, I often takes 4-5 hours. I marvel at the output of folks like Carbsane Evelyn.
I’m in favor of whichever paradigm is most helpful to patients.
My initial impression of the macrobiotic diet is that it’s vegan or vegetarian. Is that correct? At one of my other blogs I looked at the potential advantages of vegan/vegetarian diets in the setting of diabetes, leaving open the possibility that Dr. Neal Barnard et al may be on the right track. Here’s the link: http://diabeticmediterraneandiet.com/2009/11/24/are-vegetarian-diets-any-good-for-diabetes/
Thanks for your input.
-Steve
You are correct – it’s vagan
Here’s another aspect of the fatty liver/ diabetes connection.
http://perfecthealthdiet.com/2010/11/dangers-of-a-zero-carb-diet-ii-micronutrient-deficiencies/
We have a diabesity epidemic under conditions that existed previously – easy access to cheap refined carbohydrate. Which was not great for overall health or life expectancy, but only produced diabesity in a relatively few vulnerable people.
But there’s one new condition that tracks the epidemic – the availability of cheap, “heart healthy”, liver-fattening, and choline-deficient cooking oil.
Stumbled onto your blog here. Question: I know the Paleo diet tends to fall on the side of eating higher/high fat, and incorporating more into one’s diet in general. This study, and the bullet points you posted seem to vilify fats and encourage a low-calorie diet, which often goes against the creed of most Paleo dieters.
I’ve read over and and over that lowering carbohydrates is the key when it comes to controlling Diabetes – that fat is often not the villain we imagine it to be. How do you reconcile this study with the Paleo diet?
(although I did see that you still concluded a ketogenic diet was probably better than Dr. Taylor’s program. And for the record, I believe not all 11 participants remained “cured” from Diabetes several months later.)
Hi, Sara.
The Taylor program doesn’t have anything to do with the paleo diet or low-carb eating. I just thought my regular readers here might find it interesting.
On second thought, Taylor’s 600-calorie/day program quite likely is low-carb, low-fat, and low-protein.
-Steve