Given the number of threads on the forum from people experiencing reduced insulin sensitivity or weight gain on Peatarian diet I thought that I post some threads on how these conditions can be ameliorated by specific substances that Peat has written about. This thread is about vitamin B7 (biotin) and lists both human and animal studies.
The human dosages based on human and animal studies, shown to have effect on blood glucose and insulin sensitivity are in the range of 2mg-15mg daily. That seems quite high, but biotin is reportedly non-toxic even in doses 10 times higher, and so far no adverse effects have been reported in the human trials with dosages of 15mg daily. So, taking 2mg-3mg biotin daily should be fairly safe and should be enough to have an effect on blood glucose levels and insulin resistance. In addition, biotin has been shown to reduce lipogenesis and reduce fat weight of diabetic animals, while having no adverse effects on muscle.
The next threads will be on vitamin B1 (thiamine) and B6 (riboflavin) as they both have an effect on both blood glucose and insulin sensitivity.
1. Reviews of biotin
http://www.ncbi.nlm.nih.gov/pubmed/15992682
http://www.ncbi.nlm.nih.gov/pubmed/15992683
http://www.ncbi.nlm.nih.gov/pubmed/14690760
http://www.ncbi.nlm.nih.gov/pubmed/10466187
http://www.ncbi.nlm.nih.gov/pubmed/10416947
http://www.ncbi.nlm.nih.gov/pubmed/20869286
2. Human studies of biotin
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679599/
http://www.ncbi.nlm.nih.gov/pubmed/8820510
http://www.ncbi.nlm.nih.gov/pubmed/14749229
http://www.ncbi.nlm.nih.gov/pubmed/17109595
http://www.ncbi.nlm.nih.gov/pubmed/17496732
http://www.ncbi.nlm.nih.gov/pubmed/17506119
http://www.ncbi.nlm.nih.gov/pubmed/17684468
3. Animal studies of biotin
http://www.ncbi.nlm.nih.gov/pubmed/14741710
"...When islets were stimulated with glucose plus biotin, the ATP/ADP ratio increased to approximately 160% of the ATP/ADP ratio in islets stimulated with glucose alone. The rate of glucose oxidation, assessed by CO(2) production, was also about 2-fold higher in islets treated with biotin. These increasing effects of biotin were proportional to the effects seen in insulin secretion. There are no previous reports of vitamins, such as biotin, directly affecting ATP synthesis. Our data indicate that biotin enhances ATP synthesis in islets following the increased rate of substrate oxidation in mitochondria and that, as a consequence of these events, glucose-induced insulin release is reinforced by biotin.
http://www.ncbi.nlm.nih.gov/pubmed/11833042
http://www.ncbi.nlm.nih.gov/pubmed/9268917
http://www.ncbi.nlm.nih.gov/pubmed/9089478
http://www.ncbi.nlm.nih.gov/pubmed/3280936
http://www.ncbi.nlm.nih.gov/pubmed/1171166
"...Estrogen stimulated the enzyme activity in all these organs but adrenal. The study suggests that the primary reason for an acute dose of biotin-induced loss of pregnancy is blockage of estrogen production, which probably regulates endogenous progesterone secretion. The associated metabolic derangements are probably secondary to estrogen deficiency and are discussed."
http://www.ncbi.nlm.nih.gov/pubmed/15539296
http://www.ncbi.nlm.nih.gov/pubmed/18460817
http://www.ncbi.nlm.nih.gov/pubmed/20655901
http://www.ncbi.nlm.nih.gov/pubmed/22218395
http://www.ncbi.nlm.nih.gov/pubmed/22841397
http://www.ncbi.nlm.nih.gov/pubmed/23211098
The human dosages based on human and animal studies, shown to have effect on blood glucose and insulin sensitivity are in the range of 2mg-15mg daily. That seems quite high, but biotin is reportedly non-toxic even in doses 10 times higher, and so far no adverse effects have been reported in the human trials with dosages of 15mg daily. So, taking 2mg-3mg biotin daily should be fairly safe and should be enough to have an effect on blood glucose levels and insulin resistance. In addition, biotin has been shown to reduce lipogenesis and reduce fat weight of diabetic animals, while having no adverse effects on muscle.
The next threads will be on vitamin B1 (thiamine) and B6 (riboflavin) as they both have an effect on both blood glucose and insulin sensitivity.
1. Reviews of biotin
http://www.ncbi.nlm.nih.gov/pubmed/15992682
http://www.ncbi.nlm.nih.gov/pubmed/15992683
http://www.ncbi.nlm.nih.gov/pubmed/14690760
http://www.ncbi.nlm.nih.gov/pubmed/10466187
http://www.ncbi.nlm.nih.gov/pubmed/10416947
http://www.ncbi.nlm.nih.gov/pubmed/20869286
2. Human studies of biotin
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3679599/
http://www.ncbi.nlm.nih.gov/pubmed/8820510
http://www.ncbi.nlm.nih.gov/pubmed/14749229
http://www.ncbi.nlm.nih.gov/pubmed/17109595
http://www.ncbi.nlm.nih.gov/pubmed/17496732
http://www.ncbi.nlm.nih.gov/pubmed/17506119
http://www.ncbi.nlm.nih.gov/pubmed/17684468
3. Animal studies of biotin
http://www.ncbi.nlm.nih.gov/pubmed/14741710
"...When islets were stimulated with glucose plus biotin, the ATP/ADP ratio increased to approximately 160% of the ATP/ADP ratio in islets stimulated with glucose alone. The rate of glucose oxidation, assessed by CO(2) production, was also about 2-fold higher in islets treated with biotin. These increasing effects of biotin were proportional to the effects seen in insulin secretion. There are no previous reports of vitamins, such as biotin, directly affecting ATP synthesis. Our data indicate that biotin enhances ATP synthesis in islets following the increased rate of substrate oxidation in mitochondria and that, as a consequence of these events, glucose-induced insulin release is reinforced by biotin.
http://www.ncbi.nlm.nih.gov/pubmed/11833042
http://www.ncbi.nlm.nih.gov/pubmed/9268917
http://www.ncbi.nlm.nih.gov/pubmed/9089478
http://www.ncbi.nlm.nih.gov/pubmed/3280936
http://www.ncbi.nlm.nih.gov/pubmed/1171166
"...Estrogen stimulated the enzyme activity in all these organs but adrenal. The study suggests that the primary reason for an acute dose of biotin-induced loss of pregnancy is blockage of estrogen production, which probably regulates endogenous progesterone secretion. The associated metabolic derangements are probably secondary to estrogen deficiency and are discussed."
http://www.ncbi.nlm.nih.gov/pubmed/15539296
http://www.ncbi.nlm.nih.gov/pubmed/18460817
http://www.ncbi.nlm.nih.gov/pubmed/20655901
http://www.ncbi.nlm.nih.gov/pubmed/22218395
http://www.ncbi.nlm.nih.gov/pubmed/22841397
http://www.ncbi.nlm.nih.gov/pubmed/23211098