The paper that Mendosa refers to:
http://diabetes.diabetesjournals.org/cgi/reprint/49/4/640
"Increase in Fat Oxidation on a High-Fat
Diet Is Accompanied by an Increase in
Triglyceride-Derived Fatty Acid Oxidation"

Includes this detail on
"Diets . The low-fat diets consisted of 30% energy as fat,
55% energy as carbohydrate, and 15% energy as protein. The
high-fat diets consisted of 60% energy as fat, 25% energy as
carbohydrate, and 15% energy as protein. Before the
experiment, subjects filled out a 3-day food intake record
to estimate habitual dietary intake. Metabolizable energy
intake and macronutrient composition of the diet was
calculated using the Dutch food composition table (13). On
days 1 and 2 and the first part of day 3, a low-fat diet for
consumption at home was provided. Subjects were given a
fixed amount of food (based on their food intake record) and
ad libitum access to low-fat snacks. On the evening of day
3, subjects consumed their dinner and evening snack (either
low- or high-fat) in the respiration chamber. In the LF and
HF treatment, energy intake for dinner and evening snack was
fixed at 35% and 10% of estimated daily energy expenditure
(1.7 · basic metabolic rate based on the Harris and Benedict
equations [14]). In the HF1+EX treatment, the evening snack
had an energy content equal to energy expended during the
exercise test. On day 4, subjects were given an amount of
energy equal to 1.55 times the sleeping metabolic rate, as
measured during the preceding night. In a previous study, we
showed that with a comparable activity protocol used in the
chamber, a physical activity index of 1.58 was reached (4).
Subjects were asked not to consume any products with a high
abundance of 1 3C (carbohydrates derived from C4 plants like
corn and sugar cane) 1 week before and during the entire
experimental period."

There is an interesting Table 4 which compares the seven
subjects at the start of each phase of the study. If we make
the assumption that the phases were consecutive (I accept
that may be a false assumption although it appears valid
from the discussion) then the start points after the Low-fat
phase were:

Glucose (mmol/l) 5.10 ± 0.23
Insulin (µU/ml) 5.5 ± 2.0
Triglycerides (µmol/l) 556 ± 66
Fatty acids (µmol/l)  401 ± 64

A progressive improvement after each phase is noticeable,
but most improvement occurred after the high fat stages.
The start point after two of the high fat phases, prior to
the final phase were:

Glucose (mmol/l) 4.84 ± 0.13
Insulin (µU/ml) 3.5 ± 0.5
Triglycerides (µmol/l) 454 ± 55
Fatty acids (µmol/l)  385 ± 50

Possibly that answers your question "what effect will
increasing fats have on lipids?", at least partially.
Triglycerides and Fatty Acids went down, not up.

Ask them. Mendosa has a section for comments on the blog. He
is quite approachable. I'll watch for your comment.

Cheers, Alan, T2, Australia.
d&e, metformin 1500mg, ezetrol 10mg
Everything in Moderation - Except Laughter.
--
http://loraldiabetes.blogspot.com

Bernstein's people were a) on insulin and b) trying to gain weight.
Excess insulin acts by storing excess carbs as fat, and preventing fat
stores in the body being burnt because it prepares cells to burn
glucose, not fatty acids. Bernstein's experiment shows that the
addition of fats - a whopping 900 extra calories a day - has no effect
on weight in the presence of insulin.

Mendosa's interest is that he low-spikes and high exercises; he
doesn't have much excess insulin or insulin resistance. By eating a
higher fat diet, he can increase the use his body makes of fatty acids
because his levels of insulin-sensitive lipase will go up. He should
be using fat from stores, and therefore lose weight.

It will improve the lipid profile from a diet containing carbs in
greater than ketosis quantities, because all the regulating mechanisms
will be able to function without those pesky carbs. Specifically,
trigs should plummet, because there will be insufficient glucose
burning to form the basis of the tri-glyceride molecule.

What do you think a good fat is?

Nicky.
T2 dx 05/04 + underactive thyroid
D&E, 100ug thyroxine
Last A1c 5.6%  BMI 25