How do Your Genes Affect Obesity and Diabetes Supplement

A popular area of research is to determine genetic causes of obesity, diabetes, heart disease, autoimmune disease, depression and any other illness or condition that is plaguing our society. Proposed genetic solutions will result in expensive and profit-driven procedures that do not solve the primary cause of the problem.

This area of research ignores the fact that often our genetic code does not determine health outcomes and it will not solve the problems of our society’s rapidly failing health.

Frequently the problem is not that complicated.

An allele is one of two or more versions of a gene. An individual inherits two alleles for each gene, one from each parent.

The most familiar alleles relates to those that determine the ABO blood groups. The ABO blood groups are controlled by a gene that has 6 alleles (O, A, B) – 3 from each parent. Each person can have a gene consisting of the alleles OO, OA, OB, AA, BB or AB. This results in the blood groups O, A, B, A, B, AB since A and B alleles are dominant over the recessive O.

Below are the supplementary data bases associated with the Diet Intervention Examining The Factors Interacting with Treatment Success (DIETFITS) is a clinical trial.

The following table shows the baseline values at the start of the study and the changes after the study was completed at 12 months.

Criteria	Units	Low-fat diet			Low-carb diet
		Baseline	12 month Change	% Change	Baseline	12 month Change	% Change
Weight	kg	97.5	-5.29	-5.4	96.3	-5.99	6.2
BMI	kg/(m * m)	33.4	-1.75	-5.2	33.3	-2.07	-6.3
HDL	mmol/L	1.28	0	0	1.29	0.1	7.8
LDL	mmol/L	2.89	-0.1	-3.4	2.94	0.1	3.4
Triglycerides	mmol/L	1.45	-0.11	-7.5	1.45	0.32	22.1
Blood pressure (systolic)	mmHg	122.9	-3.18	-2.6	122.9	-3.72	-3.0
Fasting glucose	mmol/L	5.5	-0.2	-3.6	5.5	-0.1	-1.8
Fasting insulin	pmol/L	110	-18	-16.4	108	-16	-14.8

The following table shows how the authors grouped the genotypes into the low-fat genotype and low-carbohydrate genotype based on variants to the alleles. The variants are indicated in bold. C’ is pronounced as C prime.

Genotype	Pattern	FABP2 G > A	PPARG C > G	ADRB2 C > G	Freq %
Low Fat Genotype
Low fat	1	GA'	C'C'	CC	14
Low fat	2	GA'	C'C'	CG	14
Low fat	3	GA'	C'C'	GG	4
Low fat	4	A'A	C'C'	CC	4
Low fat	5	A'A	C'C'	CG	3
Low Carbohydrate Genotype
Low carb	6	GA	CG'	CG'	6
Low carb	7	GG	CG'	CG'	5
Low carb	8	GG	CG'	GG'	1
Low carb	9	AA	CG'	CG'	1
Low carb	10	GA	CG'	GG'	1
Low carb	11	GG	CC	CG'	19
Low carb	12	GG	CG'	CC	4
Low carb	13	GA	CG'	CC	3
Low carb	14	GG	CC	GG'	3
No Genotype
None	15	GG	CC	CC	17

The following table shows the participants with metabolic syndrome at baseline (the start of the study) and the number of participants in the each of genotype groups for the 2 diets.

Criteria	Units	Low-fat diet	Low-carb diet
Metabolic syndrome	%	34.8	32.9
Genotype - Low-fat	%	42.6	37.5
Genotype - Low-carb	%	27.2	31.9
Genotype - None	%	23.0	25.0

The following table shows the change in the metabolic syndrome status after 12 months, for the 2 diets.

Criteria	At start	After 12 months	Low-fat diet	Low-carb diet
Metabolic syndrome	Yes	No	11.8%	11.8%
Metabolic syndrome	Yes	Yes	12.8%	11.8%
Metabolic syndrome	No	No	42.0%	45.1%
Metabolic syndrome	No	Yes	4.3%	3.6%

Last two columns indicate the percentage of people that meet the conditions of the first three columns after 12 months

Only 12% of the participants were able to overcome their metabolic syndrome after 12 months on either of the two diets
12% of the participants were unable to overcome their metabolic syndrome after 12 months on either of the two diets
4.3% of the participants on the Low-fat diet and 3.6% on the Low-carb diet managed to acquire their metabolic syndrome condition after 12 months