Waves G, sorry you're not feeling well
Thank you for your kind words re.our Facebook page- a labor of love. All, please check it out if you're not in the habit. It's chockfull of non-controversial strategies and current AD/ApoE4 news. I'm no longer double posting there & here due to time restraints: https://www.facebook.com/apoe4.info?ref=ts&fref=ts
When you mentioned "isocaloric" I immediately thought if the same set of studies that Russ referenced because of their very controlled nature. The result of one will be available around Christmas. It should be telling. But, Ski has an excellent point. Until we have a RCT with E4 subjects,
we can only try to glean pertinent information that may or may not apply to us. A cursory search of published research reveals two such supposedly isocaloric studies.
Here's a large meta-analysis of 19 different randomized trials, 316 subjects, that pitted LFHC vs HFLC isocaloric diets. The results (underlined below/my emphasis) indicate a generally worsened atherogenic profile on LFHC. Keep in mind, these subjects were type 2 diabetics and APOE status wasn't stratified. Influence of Fat and Carbohydrate Proportions on the Metabolic Profile in Patients With Type 2 Diabetes: A Meta-Analysishttp://care.diabetesjournals.org/content/32/5/959.full
RESULTS Changes in values for A1C, fasting plasma glucose (FPG), and total and LDL cholesterol did not differ significantly between the LFHC (24% F/58% C) and HFLC (40%F/40% carbs) groups. However, the LFHC diet significantly increased fasting insulin and triglycerides by 8% (P = 0.02) and 13% (P < 0.001), respectively, and lowered HDL cholesterol by 6% (P < 0.001) compared with the HFLC diet.
There were positive associations among the magnitude of changes in FPG, fasting insulin, and triglycerides for the diets analyzed. However, stratified analysis indicated that the increase in triglycerides was insignificant when accompanied by energy intake restriction.
Here's another supposedly isocaloric comparison of the two approaches with a hypocaloric twist. This was much smaller; 55 subjects, who were identified as obese, but otherwise healthy. When both groups concurrently practiced CR, the results were less dramatic, but the HFLC group still
prevailed in decreases in TGs, CRP, and increases in HDL and adiponectin.Consuming a hypocaloric high fat low carbohydrate diet for 12 weeks lowers C-reactive protein, and raises serum adiponectin and high density lipoprotein-cholesterol in obese subjectshttp://www.sciencedirect.com/science/ar ... 9513002230
The age range of subjects was 21–62 years. As a percentage of daily calories, the HFLC group consumed 33.5% protein, 56.0% fat and 9.6% carbohydrate and the LFHC group consumed 22.0% protein, 25.0% fat and 55.7% carbohydrate. The change in percent body weight, lean and fat mass, blood pressure, flow mediated dilation, hip:waist ratio, hemoglobin A1C, fasting insulin and glucose, and glucose and insulin response to a 2 h oral glucose tolerance test did not differ (P > 0.05) between diets after 12 weeks. The HFLC group had greater mean decreases in serum triglyceride (P = 0.07), and hs-CRP (P = 0.03), and greater mean increases in HDL cholesterol (P = 0.004), and total adiponectin (P = 0.045) relative to the LFHC. Secreted adipose tissue adiponectin or TNF-α did not differ after weight loss for either diet.
It's very interesting to note that many of the advantages of the HFLC dwindle when compared to a hypocaloric LFHC diet. STILL, the evidence leans towards HFLC as improving IR and increasing HDL- BOTH of which have been implicated as important strategies in AD prevention- especially for E4 carriers.
However, If that benefit comes at a cost of driving up LDL-C/LDL-P...we must carefully weigh our strategies. I see lots of very smart members here hedging their bets in both directions until more evidence becomes available.