Saturated fats makes you stupid?

Rodents:
One-month-old rats were fed 1 of 4 high-fat diets (20% fat) or chow (4.5% fat) for 3 months. Dietary saturated (SFA), monounsaturated (MUFA), or polyunsaturated (PUFA) fatty acids varied such that their independent effects on cognitive performance could be tested. Rats were tested on a variable-interval delayed-alternation task. Impairment in both the ability to learn the basic alternation rule and remembering trial-specific information over time was observed in rats fed the experimental diets relative to those fed chow. The degree of impairment was highly associated with the level of SFAs fed and independent of the MUFAs or PUFAs. Dietary fat altered brain phosphatidylcholine fatty-acid profile, but the membrane changes did not correlate with cognitive impairment. The results demonstrate that cognitive impairment is directly associated with SFA intake but suggest that the mechanism is independent of bulk brain membrane compositional changes.
http://www.ncbi.nlm..../pubmed/8888990


Humans
BACKGROUND: Few studies have investigated the effects of dietary fats on the development of Alzheimer disease. We examined the associations between intake of specific types of fat and incident Alzheimer disease in a biracial community study. METHODS: We performed clinical evaluations on a stratified random sample of 815 community residents aged 65 years and older who were unaffected by Alzheimer disease at baseline and who completed a food-frequency questionnaire a mean of 2.3 years before clinical evaluation. RESULTS: After a mean follow-up of 3.9 years, 131 persons developed Alzheimer disease. Intakes of saturated fat and trans-unsaturated fat were positively associated with risk of Alzheimer disease, whereas intakes of omega-6 polyunsaturated fat and monounsaturated fat were inversely associated. Persons in the upper fifth of saturated-fat intake had 2.2 times the risk of incident Alzheimer disease compared with persons in the lowest fifth in a multivariable model adjusted for age, sex, race, education, and apolipoprotein E epsilon4 allele status (95% confidence interval, 1.1-4.7). Risk also increased with consumption of trans-unsaturated fats, beginning with the second fifth of intake (relative risk, 2.4 compared with the lowest fifth; 95% confidence interval, 1.1-5.3). We observed linear inverse associations between Alzheimer disease and vegetable fat (P =.002), and, after further adjustment for other types of fat, marginally significant associations with intake of omega-6 polyunsaturated fat (P =.10 for trend) and monounsaturated fat (P =.10 for trend). Intakes of total fat, animal fat, and dietary cholesterol were not associated with Alzheimer disease. CONCLUSION: High intake of unsaturated, unhydrogenated fats may be protective against Alzheimer disease, whereas intake of saturated or trans-unsaturated (hydrogenated) fats may increase risk.
http://www.ncbi.nlm....pubmed/12580703

Background: Lifestyle and vascular factors have been linked to dementia and Alzheimer's disease (AD), but the role of dietary fats in the development of dementia is less clear. Methods: Participants were derived from random, population-based samples initially studied in midlife (1972, 1977, 1982, or 1987). Fat intake from spreads and milk products was assessed using a structured questionnaire and an interview. After an average follow-up of 21 years, a total of 1,449 (73%) individuals aged 65-80 years participated in the re-examination in 1998. Altogether 117 persons had dementia. Results: Moderate intake of polyunsaturated fats at midlife decreased the risk of dementia even after adjustment for demographic variables, other subtypes of fats, vascular risk factors and disorders, and apolipoprotein E (ApoE) genotype (OR 0.40, CI 0.17-0.94 for the 2nd quartile vs. 1st quartile), whereas saturated fat intake was associated with an increased risk (OR 2.45, CI 1.10-5.47 for the 2nd quartile). The associations were seen only among the ApoE 4 carriers. Conclusions: Moderate intake of unsaturated fats at midlife is protective, whereas a moderate intake of saturated fats may increase the risk of dementia and AD, especially among ApoE4 carriers. Thus, dietary interventions may potentially modify the risk of dementia, particularly among genetically susceptible individuals.

BACKGROUND: Evidence from prospective epidemiologic studies and animal models suggests that intakes of dietary fats and copper may be associated with neurodegenerative diseases. OBJECTIVE: To examine whether high dietary copper intake is associated with increased cognitive decline among persons who also consume a diet high in saturated and trans fats. DESIGN: Community-based prospective study. SETTING: Chicago, Ill.Patients Chicago residents 65 years and older. MAIN OUTCOME MEASURES: Cognitive function was assessed using 4 cognitive tests administered during in-home interviews at 3-year intervals for 6 years. Dietary assessment was performed with a food frequency questionnaire. Dietary intakes of copper and fats were related to change in global cognitive score (the mean of the 4 tests) among 3718 participants. RESULTS: Among persons whose diets were high in saturated and trans fats, higher copper intake was associated with a faster rate of cognitive decline. In multiple-adjusted mixed models, the difference in rates for persons in the highest (median, 2.75 mg/d) vs lowest (median, 0.88 mg/d) quintiles of total copper intake was -6.14 standardized units per year (P<.001) or the equivalent of 19 more years of age. There was also a marginally statistically significant association (P = .07) with the highest quintile of food intake of copper (median, 1.51 mg/d) and a strong dose-response association with higher copper dose in vitamin supplements. Copper intake was not associated with cognitive change among persons whose diets were not high in these fats. CONCLUSION: These data suggest that high dietary intake of copper in conjunction with a diet high in saturated and trans fats may be associated with accelerated cognitive decline.
http://www.ncbi.nlm....pubmed/16908733

OBJECTIVE: To examine whether consumption of different types of fat is associated with age-related change in cognition. METHODS: The authors related fat consumption to 6-year change in cognitive function among 2,560 participants of the Chicago Health and Aging Project, ages 65 and older, with no history of heart attack, stroke, or diabetes at baseline. Fat intake was measured by food frequency questionnaire. Cognitive function was measured at baseline and 3-year and 6-year follow-ups, using the average z score of four cognitive tests: the East Boston Tests of Immediate and Delayed Recall, the Mini-Mental State Examination, and the Symbol Digit Modalities Test. RESULTS: In separate mixed models adjusted for demographic and cardiovascular risk factors and intakes of antioxidant nutrients and other dietary fats, higher intakes of saturated fat (p for trend = 0.04) and trans-unsaturated fat (p for trend = 0.07) were linearly associated with greater decline in cognitive score over 6 years. These associations became stronger in analyses that eliminated persons whose fat intake changed in recent years or whose baseline cognitive scores were in the lowest 15%. Inverse associations with cognitive decline were observed in these latter restricted analyses for high intake of monounsaturated fat and a high ratio of polyunsaturated to saturated fat intake. Intakes of total fat, vegetable and animal fats, and cholesterol were not associated with cognitive change. CONCLUSION: A diet high in saturated or trans-unsaturated fat or low in nonhydrogenated unsaturated fats may be associated with cognitive decline among older persons.
http://www.ncbi.nlm....pubmed/15136684

Edited by Blue, 16 October 2009 - 09:09 AM.

I don't see how this would be physiologically the case, seeing as a high intake of PUFAs would cause ALEs in the brain. Why do they lump saturated fats and trans-unsaturated fats together, as if they were somehow related? If someone is consuming high amounts of both then it suggests to me there's a bad diet going on in general.

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I don't see how this would be physiologically the case, seeing as a high intake of PUFAs would cause ALEs in the brain. Why do they lump saturated fats and trans-unsaturated fats together, as if they were somehow related? If someone is consuming high amounts of both then it suggests to me there's a bad diet going on in general.

As far as I see they do not lump saturated fats and trans-unsaturated fats together. Both are related separately to cognitive decline.

Here is another study. In this fat type does not affect dementia but saturated is less good for Parkinson:

OBJECTIVE: To examine whether high intake of total fat, saturated fatty acids (saturated fat), trans fatty acids (trans fat), and cholesterol and low intake of monounsaturated fatty acids (MUFA), polyunsaturated fatty acids (PUFA), n-6 PUFA, and n-3 PUFA are associated with increased risk of dementia and its subtypes. METHOD: Data from the Rotterdam Study, a prospective cohort study among elderly, were used. At baseline (1990 to 1993), 5,395 subjects had normal cognition, were noninstitutionalized, and underwent complete dietary assessment by a semiquantitative food-frequency questionnaire. The cohort was continuously monitored for incident dementia, and re-examinations were performed in 1993 to 1994 and 1997 to 1999. The association between fat intake and incident dementia was examined by Cox's proportional hazards models. RESULTS: After a mean follow-up of 6.0 years, 197 subjects developed dementia (146 AD, 29 vascular dementia). High intake of total, saturated, trans fat, and cholesterol and low intake of MUFA, PUFA, n-6 PUFA, and n-3 PUFA were not associated with increased risk of dementia or its subtypes. Rate ratios of dementia per standard deviation increase in intake were for total fat 0.93 (95% CI 0.81 to 1.07), for saturated fat 0.91 (95% CI 0.79 to 1.05), for trans fat 0.90 (95% CI 0.77 to 1.06), for cholesterol 0.93 (95% CI 0.80 to 1.08), for MUFA 0.96 (95% CI 0.84 to 1.10), for PUFA 1.05 (95% CI 0.80 to 1.38), for n-6 PUFA 1.03 (95% CI 0.77 to 1.36), and for n-3 PUFA 1.07 (95% CI 0.94 to 1.22). CONCLUSION: High intake of total, saturated, and trans fat and cholesterol and low intake of MUFA, PUFA, n-6 PUFA, and n-3 PUFA were not associated with increased risk of dementia or its subtypes.
http://www.ncbi.nlm....pubmed/12499483

BACKGROUND: Unsaturated fatty acids are important constituents of neuronal cell membranes and have neuroprotective, antioxidant, and anti-inflammatory properties. OBJECTIVE: To determine if a high intake of unsaturated fatty acids might be associated with a lower risk of Parkinson disease (PD). METHODS: In the Rotterdam Study, a prospective population-based cohort study of people ages > or =55, the association between intake of unsaturated fatty acids and the risk of incident PD was evaluated among 5,289 subjects who were free of dementia and parkinsonism and underwent complete dietary assessment at baseline. PD was assessed through repeated in-person examination, and the cohort was continuously monitored by computer linkage to medical records. The data were analyzed using Cox proportional hazards regression models. RESULTS: After a mean follow-up of 6.0 years, 51 participants with incident PD were identified. Intakes of total fat, monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (PUFAs) were significantly associated with a lower risk of PD, with an adjusted hazard ratio per SD increase of energy-adjusted intake of 0.69 (95% CI 0.52 to 0.91) for total fat, of 0.68 (95% CI 0.50 to 0.94) for MUFAs, and 0.66 (95% CI 0.46 to 0.96) for PUFAs. No associations were found for dietary saturated fat, cholesterol, or trans-fat. CONCLUSION: These findings suggest that high intake of unsaturated fatty acids might protect against Parkinson disease.
http://www.neurology...ract/64/12/2040

OBJECTIVE: To investigate the association of midlife dietary fat intake to cognitive performance, and to the occurrence of clinical mild cognitive impairment (MCI) later in life in a non-demented population. DESIGN: A longitudinal population-based study. SETTING: Populations of Kuopio and Joensuu, Eastern Finland. PARTICIPANTS AND METHODS: Participants of the CAIDE study were derived from random, population-based samples studied at midlife (1972, 1977, 1982 or 1987). After an average follow-up of 21 years, a total of 1449 (72%) individuals aged 65-80 years participated in the re-examination in 1998. Altogether 82 (5.7%) people were diagnosed as having MCI. Dietary information was collected with a structured questionnaire and an interview at midlife. MAIN OUTCOME MEASURES: MCI, global cognitive and executive functions, episodic, semantic and prospective memory and psychomotor speed. RESULTS: Abundant saturated fat (SFA) intake from milk products and spreads at midlife was associated with poorer global cognitive function and prospective memory and with an increased risk of MCI (OR 2.36, 95% CI 1.17-4.74) after adjusting for demographic and vascular factors, other fats and ApoE. On the contrary, high intake of polyunsaturated fatty acids (PUFA) was associated with better semantic memory. Also frequent fish consumption was associated with better global cognitive function and semantic memory. Further, higher PUFA-SFA ratio was associated with better psychomotor speed and executive function. CONCLUSIONS: Our data suggests that dietary fat intake at midlife affects cognitive performance and occurrence of MCI later in life. The impact of dietary interventions needs to be tested in clinical trials.
http://www.ncbi.nlm....pubmed/18188871

These are some really interesting results

I agree, but I would like to see an explanation of how fat intake might cause Parkinson's or Alzheimer's. Someone with a background in chemistry/biology want to comment on these studies?

I'd also like to understand the mechanism if mental decline is caused by saturated fat.

One thing that always comes to mind when I see studies like these is what comes with each type of fat. For example, dioxin intake would likely be high in a diet high in saturated animal fats. While I don't know if dioxins are associated with dementia, they are associated with many other diseases.

I find it interesting that most of the people in these studies were older, I also find it interesting that no other information about their diet was given.

However, these studies implies that cognitive decline could be associated with high trans-unsaturated fat or saturated fat intake AND insulin resistance (by proxy, a high carbohydrate intake).

Study: Dietary fat intake and cognitive decline in women with type 2 diabetes.
"These findings suggest that lower intakes of saturated and trans fat and higher intake of polyunsaturated fat relative to saturated fat may reduce cognitive decline in individuals with type 2 diabetes."

Study: High-fat diets, insulin resistance and declining cognitive function.
"Results from our work in rats and others findings from human epidemiologic studies demonstrate deficits in cognitive performance following chronic ingestion of high fat, high saturated fat, diets. Yet, the precise physiologic mechanism underlying these deficits is not well understood. We report that older adults with insulin resistance show remarkably similar deficits in cognitive function and respond to glucose ingestion in a comparable manner to rodents fed a high-fat diet, suggesting that insulin resistance is a probable mediator of these diet-induced deficits. As insulin resistance worsens to overt type 2 diabetes, profound deficits in cognitive functions, especially those dependent on the medial temporal lobes, are apparent in both obese Zucker rats and humans with type 2 diabetes. Unlike the older adult with insulin resistance, glucose ingestion further impairs medial temporal lobe function in adults with type 2 diabetes. Collectively, the human and rodent data point to a role of diet-induced endocrine abnormalities, including the development of insulin resistance, as mediating the cognitive deficits associated with high fat consumption."

But what about young, insulin-sensitive individuals such as children?
Study: Dietary fat intake is associated with psychosocial and cognitive functioning of school-aged children in the United States.
"Overall, total fat and saturated fat were unrelated to measures of cognitive and psychosocial functioning."

The obvious explanation (well, maybe not obvious to paleos) is that saturated fat increases CVD which in turn decreases nutrition to the brain and casuses various problems.

Background. In the Seven Countries Study associations between intake of individual fatty acids and dietary cholesterol were studied in relation to serum cholesterol and 25-year mortality from coronary heart disease. All analyses concern only intercohort comparisons. Methods. In the baseline surveys carried out between 1958 and 1964, risk factors for coronary heart disease were measured among 12,763 middle-aged men constituting 16 cohorts in seven countries. In 1987 and 1988 equivalent food composites representing the average food intake of each cohort at baseline were collected locally and analyzed in a central laboratory. The vital status of all participants was verified at regular intervals during 25 years of follow-up. Results. Of the individual saturated fatty acids, the average population intake of lauric and myristic acid was most strongly related to the average serum cholesterol level (r > 0.8, P < 0.001). Strong positive associations were observed between 25-year death rates from coronary heart disease and average intake of the four major saturated fatty acids, lauric, myristic, palmitic, and stearic acid (r > 0.8, P < 0.001); the trans fatty acid elaidic acid (r = 0.78, P < 0.001); and dietary cholesterol (r = 0.55, P < 0.05). Conclusions. Interpreted in the light of experimental and clinical studies, the results of these cross-cultural analyses suggest that dietary saturated and trans fatty acids and dietary cholesterol are important determinants of differences in population rates of coronary heart disease death.
http://www.sciencedi...39d812fa5fb01dd

BACKGROUND: Metabolic studies suggest that saturated fatty acids differ in their effects on blood lipids. OBJECTIVE: The objective was to examine the associations between intakes of individual saturated fatty acids and their food sources in relation to the risk of coronary heart disease (CHD). DESIGN: This was a prospective cohort study of 80082 women in the Nurses' Health Study aged 34-59 y. Subjects had no known cardiovascular disease, cancer, hypercholesterolemia, or diabetes, and completed validated food-frequency questionnaires in 1980. RESULTS: During 14 y of follow-up, we documented 939 incident cases of major CHD events. In multivariate analyses in which age, smoking, and other covariates were controlled for, intakes of short- to medium-chain saturated fatty acids (4:0-10:0) were not significantly associated with the risk of CHD. In contrast, intakes of longer-chain saturated fatty acids (12:0-18:0) were each separately associated with a small increase in risk. The multivariate RR for a 1% energy increase from stearic acid was 1.19 (95% CI: 1.02, 1.37). The ratio of polyunsaturated to saturated fat was strongly and inversely associated with CHD risk (multivariate RR for a comparison of the highest with the lowest deciles: 0.58; 95% CI: 0.41, 0.83; P for trend < 0.0001). Conversely, higher ratios of red meat to poultry and fish consumption and of high-fat to low-fat dairy consumption were associated with significantly greater risk. CONCLUSION: A distinction between stearic acid and other saturated fats does not appear to be important in dietary advice to reduce CHD risk, in part because of the high correlation between stearic acid and other saturated fatty acids in typical diets.
http://www.ncbi.nlm....pubmed/10584044

I find it interesting that most of the people in these studies were older, I also find it interesting that no other information about their diet was given.

However, these studies implies that cognitive decline could be associated with high trans-unsaturated fat or saturated fat intake AND insulin resistance (by proxy, a high carbohydrate intake).

Study: Dietary fat intake and cognitive decline in women with type 2 diabetes.
"These findings suggest that lower intakes of saturated and trans fat and higher intake of polyunsaturated fat relative to saturated fat may reduce cognitive decline in individuals with type 2 diabetes."

Study: High-fat diets, insulin resistance and declining cognitive function.
"Results from our work in rats and others findings from human epidemiologic studies demonstrate deficits in cognitive performance following chronic ingestion of high fat, high saturated fat, diets. Yet, the precise physiologic mechanism underlying these deficits is not well understood. We report that older adults with insulin resistance show remarkably similar deficits in cognitive function and respond to glucose ingestion in a comparable manner to rodents fed a high-fat diet, suggesting that insulin resistance is a probable mediator of these diet-induced deficits. As insulin resistance worsens to overt type 2 diabetes, profound deficits in cognitive functions, especially those dependent on the medial temporal lobes, are apparent in both obese Zucker rats and humans with type 2 diabetes. Unlike the older adult with insulin resistance, glucose ingestion further impairs medial temporal lobe function in adults with type 2 diabetes. Collectively, the human and rodent data point to a role of diet-induced endocrine abnormalities, including the development of insulin resistance, as mediating the cognitive deficits associated with high fat consumption."

But what about young, insulin-sensitive individuals such as children?
Study: Dietary fat intake is associated with psychosocial and cognitive functioning of school-aged children in the United States.
"Overall, total fat and saturated fat were unrelated to measures of cognitive and psychosocial functioning."

I am pretty certain that the epidemiological studies I cited regarding the effect of macronutrient intake corrected for the effect of other macronutrients such proteins and carbohydrates. Otherwise the authors do not deserve to be called epidemiologists.

Edited by Blue, 16 October 2009 - 06:20 PM.

Perhaps there is some implication for stearic acid:

Study: Cognitive decline and fatty acid composition of erythrocyte membranes--The EVA Study.
RESULTS: Higher proportions of both stearic acid (saturated, 18:0) and total n-6 polyunsaturated fatty acids were associated with greater risk of cognitive decline; the odds ratios were 1.91 (95% CI: 1.16, 3.15) and 1.59 (95% CI: 1.04, 2.44), respectively, for 1-SD differences in fatty acid proportions. Conversely, a higher proportion of total n-3 fatty acids was associated with a lower risk of cognitive decline; the odds ratio was 0.59 (95% CI: 0.38, 0.93).

I've seen studies indicating that SFA alters the blood vessels in the brain, and that in turn causes cognitive decline.
However, stearic acid is known to be coverted to oleic acid in the body. Oleic acid is a mono-unsaturated omega-9 fatty acid.

And according to this article (and study), oleic acid actually improves memory.

Unless you are eating butter or coconut oil by the spoonful you probably aren't getting as much saturated fat as you think. Even then a fair chunk of the lauric acid in coconut oil is converted into the mono-unsaturated fat mono-laurin.

I am pretty certain that the epidemiological studies I cited regarding the effect of macronutrient intake corrected for the effect of other macronutrients such proteins and carbohydrates. Otherwise the authors do not deserve to be called epidemiologists.

By pretty sure, does that mean you understand the processes by which SFA affect cognitive decline and the methodology that was used to correct for things such as carbohydrate and protein intake?

Here is a interesting study partially explaining how SFA could affect cognitive function (via oxidative stress in blood vessels):
Study: Impaired postprandial endothelial function depends on the type of fat consumed by healthy men.
"This study demonstrates that a stearic acid-rich fat attenuates the postprandial impairment in endothelial function compared with an oleic acid-rich fat and supports the hypothesis that postprandial lipemia impairs endothelial function via an increase in oxidative stress."

Postprandial lipemia is the appearance of fat in the blood. So what happens when we compare isocaloric low carbohydrate diets with high carbohydrates and their affect on postprandial lipemia:

Study: Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men.
"Postprandial lipemia was significantly reduced when the men consumed both diets compared with baseline, but the reduction was significantly greater after intake of the very low-carbohydrate diet."

By pretty sure, does that mean you understand the processes by which SFA affect cognitive decline

No. As I said, one likely explanation is the increased CVD from saturated fats (which required another explanation...).

Here is one explanation for why saturated fats are bad. Long saturated fats, unlike monounsaturated fats, are prone to accumulate in cells as incompletely degraded, toxic metabolites such as ceramide:

Insulin resistance occurs in 20%-25% of the human population, and the condition is a chief component of type 2 diabetes mellitus and a risk factor for cardiovascular disease and certain forms of cancer. Herein, we demonstrate that the sphingolipid ceramide is a common molecular intermediate linking several different pathological metabolic stresses (i.e., glucocorticoids and saturated fats, but not unsaturated fats) to the induction of insulin resistance. Moreover, inhibition of ceramide synthesis markedly improves glucose tolerance and prevents the onset of frank diabetes in obese rodents. Collectively, these data have two important implications. First, they indicate that different fatty acids induce insulin resistance by distinct mechanisms discerned by their reliance on sphingolipid synthesis. Second, they identify enzymes required for ceramide synthesis as therapeutic targets for combating insulin resistance caused by nutrient excess or glucocorticoid therapy.
http://www.ncbi.nlm....pubmed/17339025

Edited by Blue, 16 October 2009 - 06:42 PM.

Another study:

Multiple studies suggest that lipid oversupply to skeletal muscle contributes to the development of insulin resistance, perhaps by promoting the accumulation of lipid metabolites capable of inhibiting signal transduction.Herein we demonstrate that exposing muscle cells to particular saturated free fatty acids (FFAs), but not mono-unsaturated FFAs, inhibits insulin stimulation of Akt/protein kinase B, a serinelthreonine kinase that is a central mediator of insulin-stimulated anabolic metabolism. These saturated FFAs concomitantly induced the accumulation of ceramide and diacylglycerol, two products of fatty acyl-CoA that have been shown to accumulate in insulin-resistant tissues and to inhibit early steps in insulin signaling. Preventing de novo ceramide synthesis negated the antagonistic effect of saturated FFAs toward Akt/protein kinase B. Moreover, inducing ceramide buildup recapitulated and augmented the inhibitory effect of saturated FFAs. By contrast, diacylglycerol proved dispensable for these FFA effects. Collectively these results identify ceramide as a necessary and sufficient intermediate linking saturated fats to the inhibition of insulin signaling.
http://cat.inist.fr/...cpsidt=14645243

Another study:

Multiple studies suggest that lipid oversupply to skeletal muscle contributes to the development of insulin resistance, perhaps by promoting the accumulation of lipid metabolites capable of inhibiting signal transduction.Herein we demonstrate that exposing muscle cells to particular saturated free fatty acids (FFAs), but not mono-unsaturated FFAs, inhibits insulin stimulation of Akt/protein kinase B, a serinelthreonine kinase that is a central mediator of insulin-stimulated anabolic metabolism. These saturated FFAs concomitantly induced the accumulation of ceramide and diacylglycerol, two products of fatty acyl-CoA that have been shown to accumulate in insulin-resistant tissues and to inhibit early steps in insulin signaling. Preventing de novo ceramide synthesis negated the antagonistic effect of saturated FFAs toward Akt/protein kinase B. Moreover, inducing ceramide buildup recapitulated and augmented the inhibitory effect of saturated FFAs. By contrast, diacylglycerol proved dispensable for these FFA effects. Collectively these results identify ceramide as a necessary and sufficient intermediate linking saturated fats to the inhibition of insulin signaling.
http://cat.inist.fr/...cpsidt=14645243

This is interesting because it implicates both carbohydrate and saturated fat working synergistically to cause insulin insensitivity. FFA oversupply can only happen in skeletal muscle when the glucose is the primary energy source, otherwise all dietary fat is converted to ketones. What about ketones (another form of FFA)? We excrete excess through our urine. Since ketones are released in increasingly greater amounts as glucose is reduced, it would follow that a reduced carbohydrate diet high in saturated fat would not cause these issues. Especially since carbohydrate causes postprandial lipemia (FFA in the blood) by processing glucose through the liver.

Ketone body synthesis in the brain: possible neuroprotective effects
"Ketone bodies make an important contribution to brain energy production and biosynthetic processes when glucose becomes scarce. Although it is generally assumed that the liver supplies the brain with ketone bodies, recent evidence shows that cultured astrocytes are also ketogenic cells. Moreover, astrocyte ketogenesis might participate in the control of the survival/death decision of neural cells in at least two manners: first, by scavenging non-esterified fatty acids the ketogenic pathway would prevent the detrimental actions of these compounds and their derivatives (e.g. ceramide) on brain structure and function. Second, ketone bodies may exert pro-survival actions per se by acting as cellular substrates, thereby preserving neuronal synaptic function and structural stability. These findings support the notion that ketone bodies produced by astrocytes may be used in situ as substrates for neuronal metabolism, and raise the possibility that astrocyte ketogenesis is a neuroprotective pathway."

Edited by Skotkonung, 16 October 2009 - 07:33 PM.

This is interesting because it implicates both carbohydrate and saturated fat working synergistically to cause insulin insensitivity.

More correct would be high energy and saturated fat. I am not sure you can escape this problem on a ketogenic diet if energy intake is high. This ceramide accumulation could be a problem in all body tissues that can use fatty acids, not just the muscle.

This is interesting because it implicates both carbohydrate and saturated fat working synergistically to cause insulin insensitivity.

More correct would be high energy and saturated fat. I am not sure you can escape this problem on a ketogenic diet if energy intake is high. This ceramide accumulation could be a problem in all body tissues that can use fatty acids, not just the muscle.

If high energy is the culprit, wouldn't you also see a similar issue with carbohydrate as well? The majority of the body's tissues don't use glucose as a primary energy source, they use FFA -- regardless of dietary macro-nutrient composition.

Also, as this study mentioned, utilization of the ketogenic pathway due to lack or restriction of carbohydrate, would prevent the detrimental actions of ceramide on brain structure and function.

As for my point that most SFA are converted to un-saturated acids in the body, I was wrong. Stearic acid does covert to oleic acid in the body. Oleic acid is a mono-unsaturated omega-9 fatty acid as is not implicated in this cognitive decline. However, the transformation rate occurs at about 10%.

Study: Metabolism of dietary stearic acid relative to other fatty acids in human subjects
"The results, based on stable-isotope- tracer data, show that absorption of 18:0 is not significantly different from 16:0; percent desaturation of 18:0 to 9-cis 18:1 (9.2%) is 2.4 times higher than for 16:0 to 9-cis 16:1 (3.9%) and 9- desaturation is not greatly influenced by the amount of linoleic acid in typical US diets. Additionally, compared with 16:0, 18:0 incorporation is 30-40% lower for plasma triglyceride and cholesterol ester and approximately 40% higher for phosphatidylcholine; beta- oxidation of saturated fatty acids was slower than for unsaturated fatty acids and increasing the intake of dietary linoleic acid decreased beta-oxidation of saturated fatty acids. These results indicate that metabolic differences between 18:0 and 16:0 only partially explain the difference in the cholesterolemic effect reported for these saturated fatty acids."

I think a interesting observation would be to analyze rates of Alzheimer's or dementia in populations with traditionally high levels of saturated fat in their diet (Sweden or Iceland for example).

Edited by Skotkonung, 16 October 2009 - 08:46 PM.

I agree with the poster asking how they can lump saturateds with trans fats?

Quite frankly, there is some politics involved.

We need saturated fats for lungs, kidneys, etc.

I agree with the poster asking how they can lump saturateds with trans fats?

They did not.

This is interesting because it implicates both carbohydrate and saturated fat working synergistically to cause insulin insensitivity.

More correct would be high energy and saturated fat. I am not sure you can escape this problem on a ketogenic diet if energy intake is high. This ceramide accumulation could be a problem in all body tissues that can use fatty acids, not just the muscle.

If high energy is the culprit, wouldn't you also see a similar issue with carbohydrate as well? The majority of the body's tissues don't use glucose as a primary energy source, they use FFA -- regardless of dietary macro-nutrient composition.

Also, as this study mentioned, utilization of the ketogenic pathway due to lack or restriction of carbohydrate, would prevent the detrimental actions of ceramide on brain structure and function.

As for my point that most SFA are converted to un-saturated acids in the body, I was wrong. Stearic acid does covert to oleic acid in the body. Oleic acid is a mono-unsaturated omega-9 fatty acid as is not implicated in this cognitive decline. However, the transformation rate occurs at about 10%.

Study: Metabolism of dietary stearic acid relative to other fatty acids in human subjects
"The results, based on stable-isotope- tracer data, show that absorption of 18:0 is not significantly different from 16:0; percent desaturation of 18:0 to 9-cis 18:1 (9.2%) is 2.4 times higher than for 16:0 to 9-cis 16:1 (3.9%) and 9- desaturation is not greatly influenced by the amount of linoleic acid in typical US diets. Additionally, compared with 16:0, 18:0 incorporation is 30-40% lower for plasma triglyceride and cholesterol ester and approximately 40% higher for phosphatidylcholine; beta- oxidation of saturated fatty acids was slower than for unsaturated fatty acids and increasing the intake of dietary linoleic acid decreased beta-oxidation of saturated fatty acids. These results indicate that metabolic differences between 18:0 and 16:0 only partially explain the difference in the cholesterolemic effect reported for these saturated fatty acids."

I think a interesting observation would be to analyze rates of Alzheimer's or dementia in populations with traditionally high levels of saturated fat in their diet (Sweden or Iceland for example).

Yes, there would be problem with high carbohydrate/saturated diet. Just arguing that a low carbohydrate high saturated ketogenic diet would not solve the problem. Skip the saturated and use monounsaturated instead. Or maybe very short saturated. I am not sure that coconut is on average short enough. The neurons do not use saturated fats directly so a bad effect on the brain, if due to ceramide, likely comes from the vasculature or systemic factures such as inflammation or homones.

Replacing the saturated with carbohydrates is not what is recommended even if many think so. Carbohydrates may have problems of their own. Maybe due to the posprandial increases in lipids or glucose as you point out. From what I have seen this problem is attenuated with low GI foods.

Edited by Blue, 16 October 2009 - 09:37 PM.

Just arguing that a low carbohydrate high saturated ketogenic diet would not solve the problem. Skip the saturated and use monounsaturated instead.

By "not solve the problem" do you mean it wouldn't be relevant to most people or that it likely isn't sufficient to protect against LCTs? On the first point, I agree, a low-carbohydrate ketogenic diet is not desirable or even financially feasible for many people. These individuals may be better reducing SFAs. On the second point, I would not recommend using primarily monounsaturated fats. MCTs for example, generate more ketones than any other type of triglyceride. These ketones utilize the ketogenic path and exert a protective benefit. In this regard, fats can be healthy.

Study: A ketogenic diet reduces amyloid beta 40 and 42 in a mouse model of Alzheimer's disease
"Previous studies have suggested that diets rich in cholesterol and saturated fats increased the deposition of Aβ and the risk of developing AD. Here we demonstrate that a diet rich in saturated fats and low in carbohydrates can actually reduce levels of Aβ. Therefore, dietary strategies aimed at reducing Aβ levels should take into account interactions of dietary components and the metabolic outcomes, in particular, levels of carbohydrates, total calories, and presence of ketone bodies should be considered."

Study: Clinical Aspects of the Ketogenic Diet
"Animal models of Alzheimer's disease and amyotrophic lateral sclerosis have shown benefit from the ketogenic diet (Van der Auwera, 2005; Zhao et al., 2006)."

Study: Neuroprotective and disease-modifying effects of the ketogenic diet
"Recent studies have raised the possibility that the ketogenic diet could provide symptomatic benefit and might even be disease modifying in Alzheimer's disease. Thus, Reger et al. (2004) found that acute administration of medium-chain triglycerides improves memory performance in Alzheimer's disease patients. Further, the degree of memory improvement was positively correlated with plasma levels of β-hydroxybutyrate produced by oxidation of the medium-chain triglycerides. If β-hydroxybutyrate is responsible for the memory improvement, then the ketogenic diet, which results in elevated β-hydroxybutyrate levels, would also be expected to improve memory function. When a patient is treated for epilepsy with the ketogenic diet, a high carbohydrate meal can rapidly reverse the antiseizure effect of the diet (Huttenlocher, 1976). It is therefore of interest that high carbohydrate intake worsens cognitive performance and behavior in patients with Alzheimer's disease (Henderson, 2004; Young et al., 2005).
It is also possible that the ketogenic diet could ameliorate Alzheimer's disease by providing greater amounts of essential fatty acids than normal or high carbohydrate diets (Cunnane et al., 2002; Henderson, 2004). This is because consumption of foods or artificial supplements rich in essential fatty acids may decrease the risk of developing Alzheimer's disease (Ruitenberg et al., 2001; Barberger-Gateau et al., 2002; Morris et al., 2003a, b)."

Study: [i]Ketone Bodies as a Therapeutic for Alzheimer's Disease
[i]"An early feature of Alzheimer's disease (AD) is region-specific declines in brain glucose metabolism. Unlike other tissues in the body, the brain does not efficiently metabolize fats; hence the adult human brain relies almost exclusively on glucose as an energy substrate. Therefore, inhibition of glucose metabolism can have profound effects on brain function. The hypometabolism seen in AD has recently attracted attention as a possible target for intervention in the disease process. One promising approach is to supplement the normal glucose supply of the brain with ketone bodies (KB), which include acetoacetate, β-hydroxybutyrate, and acetone. KB are normally produced from fat stores when glucose supplies are limited, such as during prolonged fasting. KB have been induced both by direct infusion and by the administration of a high-fat, low-carbohydrate, low-protein, ketogenic diets. Both approaches have demonstrated efficacy in animal models of neurodegenerative disorders and in human clinical trials, including AD trials. Much of the benefit of KB can be attributed to their ability to increase mitochondrial efficiency and supplement the brain's normal reliance on glucose. Research into the therapeutic potential of KB and ketosis represents a promising new area of AD research."

Clearly the issue of saturated fats and cognitive decline is not black and white. We are dealing with a complex system and I think saturated fats can both be beneficial and harmful in context of other macro-nutrients.

Edited by Skotkonung, 16 October 2009 - 10:01 PM.

Interesting thread!

Here is an interesting connection -- Barry groves gave us these stats for lowland gorillas'

Overall energy
(kcal) per 100g %age
Protein 47.1 24.3%
Available carbs 30.6 15.8%
Fat 4.9 2.5%
SCFA from fibre 111.0 57.7%

While I might consider the protein a bit high -- most of the protein is in the form of plant material which is low in methionine.

Barry used these stats to argue that most primates' diets are high in saturated fat. I have no argument with this, but what low carbers among you eat acetic, proprionic and butyric acids as their primary fats?

In fact, a lot of low carbers who read his site took this to mean they could eat a lot of the 16:0 18:0 fats. I believe this might be dangerous. The only saturated fat I consider to be semi-innocuous is coconut oil -- because its' fats don't mess with our tissues ratios much -- but it might have other unknown negative effects -- I can attest that "my body" never fully felt right on coconut oil. Might have to do with the effect of forcing the body to use fat for fuel over glucose <----- which I don't believe your body should do 100% of the time (think ketosis).

I have mentioned before that fats usually don't just get converted to energy, even on a keto diet -- they are usually put into tissue first, and then pulled out for usuage -- this could be dangerous if there is a buildup of saturated fats in the tissues that is out of the standard operating parameters for our cells.

I wont argue that carbs increase appetite -- but if you dont overeat, not much fat does to de novo lipogenesis -- Not much at all!

Edited by HaloTeK, 16 October 2009 - 10:13 PM.

Here is an interesting connection -- Barry groves gave us these stats for lowland gorillas'

Yeah, I don't know how accurate a dietary comparison between a gorilla and a human would be, seeing as we diverged evolutionarily several million years ago. They don't even share our genus.

Here is an interesting connection -- Barry groves gave us these stats for lowland gorillas'

Yeah, I don't know how accurate a dietary comparison between a gorilla and a human would be, seeing as we diverged evolutionarily several million years ago. They don't even share our genus.

For you to completely disconnect info from gorillas and or other primates would be a mistake -- of course we don't have multiple stomachs like they do -- but that was our trade off for a larger brain.

Most plant eating mammals would have similar patterns of nutrient intake -- because their gut flora would convert food sources to SCFAs. Humans have to get away with others sources of dense food to make up for that -- for some reason i bet we ate lots of bone marrow <---- high in MONOs right? And tubers -- they were an easy fuel source!

To say man is highly carnivorous would be a mistake -- we can't deal with the super high protein intake -- or the nutrients that would come from eating all of the insides of an animal -- and eating blood is dangerous unless it is treated as the Masai would. We don't even eat much of the connective issues -- which is consumed in large amounts by natural meat eaters.

Just because we can derive and use selective meat/liver tissues and cook them to increase bio-availability doesn't mean its optimal.

kind of puts a damper on coconut oil. would hope this thread is not turned into another pro-paleo, anti-carb discussion.

would be nice if we could elucidate the pathway driving this SFA issue. i guess it's time to double down on olive oil...

kind of puts a damper on coconut oil. would hope this thread is not turned into another pro-paleo, anti-carb discussion.

would be nice if we could elucidate the pathway driving this SFA issue. i guess it's time to double down on olive oil...

I just know that my thinking is much clearer since ditching the heart healthy grape nuts cereal and adding three teaspoons of coconut oil to my daily diet. Lungs feel much better too.

Here is an interesting connection -- Barry groves gave us these stats for lowland gorillas'

Yeah, I don't know how accurate a dietary comparison between a gorilla and a human would be, seeing as we diverged evolutionarily several million years ago. They don't even share our genus.

For you to completely disconnect info from gorillas and or other primates would be a mistake -- of course we don't have multiple stomachs like they do -- but that was our trade off for a larger brain.

Most plant eating mammals would have similar patterns of nutrient intake -- because their gut flora would convert food sources to SCFAs. Humans have to get away with others sources of dense food to make up for that -- for some reason i bet we ate lots of bone marrow <---- high in MONOs right? And tubers -- they were an easy fuel source!

To say man is highly carnivorous would be a mistake -- we can't deal with the super high protein intake -- or the nutrients that would come from eating all of the insides of an animal -- and eating blood is dangerous unless it is treated as the Masai would. We don't even eat much of the connective issues -- which is consumed in large amounts by natural meat eaters.

Just because we can derive and use selective meat/liver tissues and cook them to increase bio-availability doesn't mean its optimal.

I actually was debating this topic with Blue in another thread. I personally think the most accurate dietary comparisons can only be made between other hominids, especially closely related hominids. Dietary information can be gained using carbon isotope studies. Your input would be welcome.
http://www.imminst.o...o...1729&st=100

Let's keep this thread on topic, though.

Sorry all mighty Skotkonung, you sure the saturated fats haven't gone to your head to make you a little inflexible? just kidding around.

I was only referencing why I thought humans may not be suited to saturated fats -- and why how it might be possible to justify the title of this topic.

I will check out the other thread.