Show her this. It's pretty simple and it's in her preferred video format. http://youtu.be/uCFZoqmKf5M

We have a pretty sophisticated audience here, but I understand what you are trying to say and sometimes the best approach to take is one that gets her over time.

There are certain words that will sit well even with a limited view CWer. For instance, tell her the primary goal of paleo eating is to eat un-PROCESSED foods similar to what you'd find out in the wild. Everyone I've ever talked to understands processing is bad, for some reason it is conventional wisdom, so play to that. If that is well received then maybe you can go for more, or wait till a different time.

Then my favorite way to proceed is with a basic understanding of genetics and natural selection. Why is it healthier to avoid unprocessed foods? Well, simply put we did not evolve to be unhealthy. Over millions of years our genetics randomly passes traits of our parents and then the best fit to survive live on as deemed by natural selection. And this happened when you could only find unprocessed food in the wild. If your body didn't have what it took to be healthy when consuming and digesting wild meat, fruit and veggies you died. Our bodies evolved around the food, not the other way around. It is why we have small stomachs when compared to other vegetarian apes (we evolved to eat energy dense meat) and why we are so smart (to strategize and catch big game). So it is easy to see why optimal health would be achieved when eating this way.

If this is understood (and it could take several conversations) then I think it will be easier to explain the chemistry once they are actually on your side. And then Denise Minger is your best bet. You can either directly show her some of her articles or describe the basic facts.

That the neolithic agents present in modern day diets that cause disease are processed sugar, wheat (you could maybe tread lightly on this one if she isn't full convinced) and excess PUFAs. Other factors are inactivity, alcohol, smoking and so on. Studies may isolate and villainize something like cholesterol or saturated fat, but only because they misinterpreted a correlation as a causation. When it is more likely that the dude who eats lots of fatty meat (usually found at a fast food joint) is also the dude that sits on the couch and has a shake to accompany the burger. Where as the people that may avoid cholesterol have other strong health habits in line; they exercise, avoid added sugar and added fat (in the form of PUFAs). Every study has a silver lining, the hard part is finding it.

Hopefully this helps, however you choose to do it I say working her slowly is the best choice. She probably thinks that way because she trusts the experts more than herself anyway. Get her to think for herself first with what she already knows is true and then convince her over time once she comes over to your side, good luck.

http://www.nap.edu/catalog.php?record_id=10490

I haven't readed the whole thing nor can find now the sections which can help you the most, some extractions noneless:

" Higher total fat diets can probably be consumed safely by active individuals while maintaining body weight. Although in longitudinal studies of weight gain, where dietary fat predicts weight gain independent of physical activity, it is important to note that physical activity may account for a greater percentage of the variance in weight gain than does dietary fat (Hill et al., 1989). Another endpoint that merits consideration is physical performance. High fat diets (69 percent of energy) do not appear to compromise endurance in trained athletes (Goedecke et al., 1999); however, athletes may not be able to train as effectively on short-term (less than 6 days) intakes of a high fat diet as on a high carbohydrate diet (Helge, 2000). This effect on training was not observed following long-term adaptation of high fat diets."

"As shown in Tables 9-5 through 9-8, no consistent significant associations have been established between dietary cholesterol intake and cancer, including lung, breast, colon, and prostate"

"The lack of consistency in observations relating dietary cholesterol intake to clinical cardiovascular disease and CHD endpoints may be due to many factors, including the limited ability to detect such effects (e.g., due to relatively small increases in LDL cholesterol concentration and inaccuracies in dietary intake data) and to the limited ability to distinguish the effects of dietary cholesterol independent of energy intake and other dietary variables that may be positively (e.g., saturated fat intake) or negatively (e.g., fiber intake) associated with dietary cholesterol and heart disease risk. Another uncertainty relates to interpreting the effects of dietary cholesterol on blood cholesterol concentrations. Evidence indicates that increased dietary cholesterol results, on average, in increased blood concentrations of both LDL and HDL cholesterol, and it is possible that the net impact on cardiovascular disease risk depends on the relative changes in these lipoproteins, as well as on other unmeasured mediators of atherogenesis. Finally, the considerable interindividual variation in lipid response to dietary cholesterol may result in differing outcomes in different populations or population subgroups."

"However, a number of other epidemiological studies have not demonstrated a significant independent relationship of dietary cholesterol intake and CHD (Esrey et al., 1996; Kromhout and de Lezenne Coulander, 1984; Pietinen et al., 1997; Posner et al., 1991). In a cohort of 43,757 male health professionals, dietary cholesterol intake was significantly related to age-adjusted risk for myocardial infarction and fatal CHD (p < 0.003 and 0.002, respectively) across cholesterol quintiles ranging from median intakes of 189 to 422 mg/d (Ascherio et al., 1996). However, the risk was attenuated with multivariate analyses (p < 0.07 and 0.03), which included other risk factors such as body mass index, smoking habits, alcohol consumption, physical activity, history of hypertension or high blood cholesterol, family history of myocardial infarction, and profession. The risk became insignificant after adjustment for fiber intake, which was reported to be significantly inversely related to CHD risk in this cohort."

Taubes GCBC answers these questions. If you read it it will help you deal with these other folks.

Just tell her that it's specifically a high intake of myristic, palmitic and lauric acids (in that order) that increase LDL-C and that a diet high in butter and cream will increase serum cholesterol far more than a "traditional" paleo diet. Additionally, you could show her this:

If that doesn't work, you can tell her that the range of serum cholesterol that corresponds least to mortality is 200-240mg/dL.