Here are my blood glucose numbers over the past three months. I have been fasting the last week so the number are lower during the fast. This is an average of 113, and a HbA1c of 5.7. The normal range for level for hemoglobin A1c is less than 6%. Note that I am still taking Metformin. I am also doing High Carb, Healthy Fats plus Intermittent Fasting.
Remission of pre-diabetes to normal glucose tolerance in obese adults with high protein versus high carbohydrate diet: randomized control trial
Results After 6 months on the HP diet, 100% of the subjects had remission of their pre-diabetes to normal glucose tolerance, whereas only 33.3% of subjects on the HC diet had remission of their pre-diabetes. The HP diet group exhibited significant improvement in (1) insulin sensitivity (p=0.001), (2) cardiovascular risk factors (p=0.04), (3) inflammatory cytokines (p=0.001), (4) oxidative stress (p=0.001), (5) increased percent lean body mass (p=0.001) compared with the HC diet at 6 months.
I’ve got a reason to celebrate today. Three months – no Insulin. So obviously I am not dead but what happened with my daily blood sugar numbers? My meter only goes to one month on the average but I downloaded the data and here’s what it looks like (averaged over three months):
All of the daily averages are in the 80-120 range. My overall average is 101.5. That works out to a HbA1C value around 5.2. I haven’t had it tested yet but would expect my value to be somewhere around that number. That is pretty great.
I also went below the 50 lb scale drop on the work scale this past week so the weight loss is going really well also.
Clothes don’t fit all that well anymore though. I need a better belt and some new pants. I’ve been wearing XL tee shirts this past week too.
Did my third three day fast this past week. I find I can do them easily starting Monday after dinner and resume eating on Thursday. I lose around four lbs on the fast but a lb or two returned after the fast. Net seems to be a couple of lbs which is better than they would be if I had not fasted.
One of the better benefits is the dip in Blood Sugar during the fast. By the third day my numbers go from the low 80’s to upper 90’s. Meter shows my averages as 101-103 for the 7 day, 14 day and 30 day. That should be an HbA1C of around the mid 5’s. Still seeing a Dawn Effect every day and a drop by dinner time.
Still doing Intermittent Fasting and LCHF. I eat on a 20 hour fast four hour eating schedule.
My work scale shows I have lost around 46 lbs so my guess is that I am down about 50 lbs in three months.
Had Mexican food last night. Did well. Here’s how I did it.
- No chips/salsa.
- Ordered fajitas. Forget the name of it (Vallerta Fajitas maybe?). Had chicken, beef, chorizo and shrimp. Very oily/greasy. Included onions, green peppers, cauliflower, broccoli. Tasted good. No chips/salsa.
- No rice.
- No beans.
- No tortillas.
Blood sugar 2 hours later was 95 (pretty much normal for me).
From the American Diabetics Association 2008 (Nutrition Recommendations and Interventions for Diabetes):
ENERGY BALANCE, OVERWEIGHT, AND OBESITY
In overweight and obese insulin-resistant individuals, modest weight loss has been shown to improve insulin resistance. Thus, weight loss is recommended for all such individuals who have or are at risk for diabetes. (A)
For weight loss, either low-carbohydrate or low-fat calorie-restricted diets may be effective in the short term (up to 1 year). (A)
For patients on low-carbohydrate diets, monitor lipid profiles, renal function, and protein intake (in those with nephropathy), and adjust hypoglycemic therapy as needed. (E)
Wow. Back when I was a newly diagnosed T2D (in 2003) they were saying LC is bad. Now it is one of the recommended diets for Diabetics. Reading on…
The optimal macronutrient distribution of weight loss diets has not been established. Although low-fat diets have traditionally been promoted for weight loss, two randomized controlled trials found that subjects on low-carbohydrate diets lost more weight at 6 months than subjects on low-fat diets (19,20). Another study of overweight women randomized to one of four diets showed significantly more weight loss at 12 months with the Atkins low-carbohydrate diet than with higher-carbohydrate diets (20a). However, at 1 year, the difference in weight loss between the low-carbohydrate and low-fat diets was not significant and weight loss was modest with both diets. Changes in serum triglyceride and HDL cholesterol were more favorable with the low-carbohydrate diets. In one study, those subjects with type 2 diabetes demonstrated a greater decrease in A1C with a low-carbohydrate diet than with a low-fat diet (20). A recent meta-analysis showed that at 6 months, low-carbohydrate diets were associated with greater improvements in triglyceride and HDL cholesterol concentrations than low-fat diets; however, LDL cholesterol was significantly higher on the low-carbohydrate diets (21).
So everything (except LDL) was better with LC. And they did not differentiate between the various LDL (small particle size vs large).
A dialog in the 2KetoDudes Facebook group has me thinking more deeply about Gluconeogenesis (GNG). One of the folks there challenged my belief that GNG is a culprit with respect to Protein consumption. The person pointed me to a site which had a couple of articles, but this was the key one to represent his POV (Protein, Gluconeogenesis, and Blood Sugar).
It is the contention of the article that for a Keogenic (LCHF) diet the effects of Gluconeogensis from protein consumption are not significant to blood glucose levels. In fact, the article argues GNG and blood glucose levels are negatively correlated.
We haven’t found any solid evidence to support the idea that excess protein is turned into glucose.
Another interesting quote:
On the input side, blood sugar can come from three sources:
– We can eat carbohydrates, and have sugar enter the blood through digestion.
– We can make glucose out of glycogen (the limited amount of glucose stored in persistent form in the liver). This process is called glycogenolysis.
– Thirdly, we can produce new glucose by GNG.
Here’s where it gets even more interesting:
Even on a keto diet, there is still a substantial proportion of glucose production from glycogenolysis. Ultimately, of course, the glycogen in keto dieters also comes from GNG that happened previously.
Here’s a different article (Effect of long-term dietary protein intake on glucose metabolism in humans).
Glucose-stimulated insulin secretion was increased in the high protein group “516 45 pmol/l vs 305 32,p = 0.012) due to reduced glucose threshold of the endocrine beta cells “4.2 0.5 mmol/l vs 4.9 0.3, p = 0.031). Endogeneous glucose output was increased by 12% “p = 0.009) at 40 pmol/l plasma insulin in the high protein group, but not at higher insulin concentration whereas overall glucose disposal was reduced.
A newly published study (Food consumption and the actual statistics of cardiovascular diseases: an epidemiological comparison of 42 European countries).
The results of our study show that high-glycaemic carbohydrates or a high overall proportion of carbohydrates in the diet are the key ecological correlates of CVD risk. These findings strikingly contradict the traditional ‘saturated fat hypothesis’, but in reality, they are compatible with the evidence accumulated from observational studies that points to both high glycaemic index and high glycaemic load (the amount of consumed carbohydrates × their glycaemic index) as important triggers of CVDs (1, 32–34). The highest glycaemic indices (GI) out of all basic food sources can be found in potatoes and cereal products (Supplementary Table 2), which also have one of the highest food insulin indices (FII) that betray their ability to increase insulin levels.
The role of the high glycaemic index/load can be explained by the hypothesis linking CVD risk to inflammation resulting from the excessive spikes of blood glucose (‘post-prandial hyperglycaemia’) (35). Furthermore, multiple clinical trials have demonstrated that when compared with low-carbohydrate diets, a low-fat diet increases plasma triglyceride levels and decreases total cholesterol and HDL-cholesterol, which generally indicates a higher CVD risk (36, 37). Simultaneously, LDL-cholesterol decreases as well and the number of dense, small LDL particles increases at the expense of less dense, large LDL particles, which also indicates increased CVD risk (27). These findings are mirrored even in the present study because cereals and carbohydrates in general emerge as the strongest correlates of low cholesterol levels.