What To Do After You've Lost 50 # ? Get Into My Genes...

What To Do After You've Lost 50 lbs:

1. Get rid of your larger-sized jeans -- donate 'em, burn 'em, give them away, t-h-r-o-w them away so you don't get any ideas
2. Buy new hot jeans, preferable anything that makes you look hotter
3. Get rid of your larger-sized undies b/c they will peak out of your sexy new(low rise) jeans.
4. Welcome the customer service you'll get (sad but true) -- the better you look the better service (even though you're the s-a-m-e cranky consumer).
5. The better the service, the bigger the spending. Get a larger wallet!

About 5yrs ago I started on a 'health' kick which started when I couldn't fit into my size 10-12 jeans. Everyone reaches their own personal 'rock bottom' at some point which starts the process of life-altering new change. My rock bottom occurred when my bottom couldn't fit. *sigh* Wish I could say it was for improving my 'fitness' or 'golf' or 'longevity' or 'primary coronary prevention'. Nope.

You wanna get into my genes?

After losing 50 lbs (low carb, working out, yoga, eliminating juice/cereal/rice) and achieving the ultimately best health ever, I would say my genes ROCK now. Can we alter our genes and genetics? (Clinton was once clobbered for saying he changed his 'genes' and after making adjustments to his diet and weight after his multiple-vessel CABG .... we wondered what (??!) was he was talking about) *heh*

It certainly is possible to optimize and out-maneuver genetic polymorphisms (and other DNA curses). With a semi-Paleo diet, inadvertently fasting intermittently (cheating with chocolate and coffee), exercise (both low and high intensity), the weight went from originally 158 to finally 108 lbs... (115 lbs now after growing 7 lbs of muscle/mammaries/hair ... they're real... and spectacular... J/K (!!)... miss my Seinfeld). My BMI is 19.4 (size 1). I started at 38% body fat (wow -- more than 1/3 of the initial weight) and now I'd estimate 19-22%. Was it hard? Let me tell you... it wasn't always easy. But it wasn't difficult once the process started. Like a rock rolling down a hill. At some point, natural laws of gravity kick in -- with big enough kicks(and other physics, such as smaller masses require shopping for smaller jeans). Psychologists say that change takes 2 weeks to occur and be reinforced.

Randomness in workouts helps me -- mixing up the intensity and varying the lengths. Boredom can't set in when the routine is constantly changing, setting new bars of achievement (instead of 2 miles, 4 miles), finding friends to join in the fun, or attending classes where you can share camaraderie (and accountability).

French culture have taught us yet another lesson (other than croissants, butter, wine, cheese and other good foods can be good for us). By consuming the right balance of foods and right portions for our specific genetics, we can extend health, longevity, and vitality to the maximum. Make the most of the interplay between personal genetics and diet. As certain genes can be turned on for optimization of health, many genes can be down-regulated and shut OFF to stop and control chronic diseases.

As Hippocrates once said "Let thy food be thy medicine, and thy medicine thy food."

No pain-au-chocolat, no gain!

(Food was probably high-carb 50-80% of daily calories-- the context would not apply necessarily to TYP-ers and therefore dietary fat effects may not extrapolate out)Features of the metabolic syndrome (MetSyn) are modulated by an interaction between the peroxisome proliferator-activated receptor-delta -87T>C polymorphism and dietary fat in French-Canadians. Robitaille J, et al. J Obes (Lond). 2007 Mar;31(3):411-7. (More on PPAR-delta later... what a fascinating receptor)

OBJECTIVE: We verified whether genetic variants in this gene are associated with the MS and whether dietary fatty acids interact with the -87TC polymorphism.

METHODS: By direct sequencing, we identified 15 variants in the PPAR-delta gene and analyses were pursued with the -87TC polymorphism for 340 subjects.

RESULTS: Metabolic variables were comparable among each genotype group. The -87TC polymorphism, fat intake and the interaction accounted, respectively for 2.2, 1.9 and 1.5% of the variance in high-density lipoprotein cholesterol (HDL-C) levels (P less than 0.05) (age, sex and energy intake were included into the model). The total cholesterol/HDL-C ratio was also modulated by a gene-diet interaction and by the -87TC polymorphism (P less than0.05). No gene-diet interaction effects were observed for other features of the MS. The age- and sex-adjusted odds ratio (OR) of exhibiting three or more features of the MS when carrying the -87C allele was 0.62 (P=0.04) compared to -87T/T. However, in subjects consuming less than 34.4% of energy from fat (median of fat consumption), the OR in carriers of the -87C allele was of 0.42 (P=0.008).

CONCLUSION: These data suggest that the PPAR-delta -87TC polymorphism may be associated with a lower risk to exhibit the MS and this association is influenced by dietary fat intake.The metabolic syndrome (MS) is influenced by genetic and environmental factors. Peroxisome proliferator-activated receptor delta (PPAR-delta), a transcription factor involved in lipid metabolism, is a candidate gene for the MS. PMID: 16953259


A certain genetic type (polymorphism) determines whether saturated fat increases apo B (and Metabolic Syndrome and thus small dense atherogenic LDL and plaque-progression) or protects against elevated apo B (et cetera). I wish I could get into my genes... but I would bet that my genes exhibit the apo B/MetSyn/atherogenic type... like the great majority of the global human population (insulin resistant with age, sedentary lifestyle, and excessive carb intake). The A94 type is impressive (A++) but unfortunately my genes probably wouldn't be so lucky. I wish I had A++ genes... but I more than make it up with A++ physical activity and food. Robitaille J, et al. Mol Genet Metab. 2004 Aug;82(4):296-303.

Plasma concentrations of apolipoprotein B are modulated by a gene--diet interaction effect between the LFABP T94A polymorphism and dietary fat intake in French-Canadian men.
Hyperapobetalipoproteinemia is a common feature of the metabolic syndrome and could result from the interaction between genetic and dietary factors. The objective of this study was to verify whether dietary fat intake interacts with the T94A polymorphism of the liver fatty acid-binding protein (LFABP) gene to modulate plasma apolipoprotein (apo) B levels. Dietary fat and saturated fat intakes were obtained by a dietitian-administered food frequency questionnaire and the LFABP T94A genotype was determined by a PCR-RFLP based method in 623 French-Canadian men recruited through the Chicoutimi Lipid Clinic (279 T94/T94, 285 T94/A94, and 59 A94/A94). The LFABP T94A polymorphism was not associated with plasma apo B levels when fat intake was not taken into consideration. However, in a model including the polymorphism, fat intake expressed as a percentage of total energy intake, the interaction term and covariates, the variance in apo B concentrations was partly explained by the LFABP T94A polymorphism (5.24%, p = 0.01) and by the LFABP T94A*fat interaction (6.25%, p = 0.005). Results were similar when saturated fat replaced fat intake in the model (4.49%, p = 0.02 for LFABP T94A and 6.43%, p = 0.004 for the interaction). Moreover, in men consuming more than 30% of energy from fat, the odds ratio for having plasma apo B levels above 1.04 g/L for A94 carriers was of 0.40 (p = 0.02) compared to T94/T94 homozygotes. Results were similar for carriers of the A94 allele consuming more than 10% of energy from saturated fat (OR: 0.32, p = 0.005).

In conclusion, T94/T94 exhibit higher apo B levels whereas carriers of the A94 allele seem to be protected against high apo B levels when consuming a high fat and saturated fat diet. These findings reinforce the importance to take into account gene-diet interactions in the prevention and management of the metabolic syndrome. PMID: 15308127