Fat is the mechanism that makes controlled-carbohydrate weight loss work. Atkins teaches you how to use fat to your advantage. When you are doing Atkins, fat is your friend, not only because it is satiating (keeps you fuller for longer), but also because it slows down the release of glucose into the blood. By moderating blood sugar swings, fat reduces carbohydrate cravings. Dietary fat, in combination with controlled-carbohydrate consumption, accelerates the burning of stored body fat. When your body uses fat, rather than glucose for fuel, the metabolic process is called lipolysis. Eating fat accelerates the burning of fat, dietary and stored.
Fats to Eat, Fats to Avoid
The kind of fat you should eat include natural, healthy fat found in olives and olive oil, seeds, nuts, seed and nut oils and butters, avocado, and oily fish such as salmon, sardines and mackerel and butter. Saturated fat, found in meats, butter and coconut oil, poses no health risk in all Phases of the program. You will burn both dietary and body fat for energy.
The kinds of fat you should avoid are trans fats—chemically altered, processed hydrogenated oils, such as some types of margarine and shortening. Look for cold-pressed or expeller-pressed oils, and store them in a dark, cool place to keep them from going rancid or oxidizing. High heat changes the molecular structure of the cell and will transform even a good fat into a trans fat, so be sure not to burn oil or allow it to smoke while cooking.
Why Low-Fat Atkins Does Not Work
If you try to do your own low-fat version of Atkins, you will not only find that you go hungry, but you also will not achieve the weight loss results of people who consume healthy fats. You wanted a biochemistry course on fat; here it is for those for the stomach for it, no pun intended:
Dietary linoleic acid (LA, n-6) plus arachidonic acid (AA, n-6) are the two sources of cellular AA in the human body. The typical North American consumes about 15,000 mg/day of LA (and converts approx. 1-2 % or 150-300 mg/day into AA via biosynthesis as a precursor). We eat only 100-200 mg of preformed AA/day. One might expect that a vegan vegetarian (who never consumes any AA) would have about half the cellular level of AA. However, the AA levels in such subjects are only moderately lower, thereby supporting the rather more efficient conversion of LA to AA when AA is not consumed. AA, when available, can exhibit feedback control/ inhibition of LA conversion to AA.
LA conversion to AA in also reduced somewhat by higher omega-3 intakes, although this is a relatively minor factor currently in North America because of our high omega-6: omega-3 (approx. 10:1) ratio. Lowering the intake of LA and/or AA plus elevating the intake of omega-3 (LNA and particularly EPA/ DHA) can all be expected to reduce the formation of AA and AA-derived eicosanoids (including pro-inflammatory leukotrienes/cytokines).
So it would seem that the best approach in people with metabolic syndrome would be to optimize the omega-6-to-3 ratio (by reducing dietary omega-6 and supplementing with omega-3s—EPA and DHA). Controlling carbs and maintaining lowered insulin levels should also help, as insulin can stimulate delta 5 desaturase and AA availability, and adding a reduction in dietary AA should also help to favorably modify the production of pro-inflammatory cytokines and eicosanoids. Avoiding trans fats should help modify lipid membrane metabolism and optimize omega-3’s influence. It would also seem that saturated fats (including lauric acid) can be included along with MUFA, but should not necessarily be the predominant dietary fat.
