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DOES SATURATED FAT CAUSE AGING AND IMPAIR MEMORY?
WHAT THE STUDIES REALLY SAY
By Chris Masterjohn
According to Dr. Oz, “. . . all sat fat speeds up aging. It does this by turning on a potentially harmful family of genes
that we docs call RAS genes. They tell your body to churn out inflammatory proteins that cause heart disease, stroke,
wrinkles, impotence and immune system slip-ups.”
There are a number of studies dating back to the 1990s showing that dietary fat can encourage mutations in RAS
genes, which appear to activate them to their carcinogenic form, but these studies implicated fish oil and corn oil rather
than saturated fat. Corn oil dose-dependently increased the activity of RAS genes and the incidence of mammary cancer
1
in mice genetically altered to express the carcinogenic form of a particular RAS gene. A case-control study published
2
in the year 2000 found that people who ate more monounsaturated fat were more likely to have mutated RAS genes.
Similar associations were noted for saturated fat and carbohydrate but they were not statistically significant. The most
3
recent study on the subject followed more than 120,000 people for over seven years and found that intakes of saturated
and monounsaturated fat at the beginning of the study had no relationship to colon cancer risk at the end of the study.
Those with higher linoleic acid intakes, however, had a higher risk of cancer if mutated RAS genes were their only genetic
risk factor. These studies clearly implicated polyunsatuturated fats rather than saturated fats.
4
Regarding claims that saturated fat impairs memory, there are three studies claiming to show that a “saturated-fat diet”
decreases levels of brain-derived neurotrophic factor (BDNF). 5,6,7 These studies used low-fat control diets providing the
majority of calories as starch and compared them to high-fat, high-sugar diets where most of the calories came from lard
and sucrose. Lard contains about ten percent of its fat as polyunsaturated fatty acids, which promote oxidative stress,
8,9
and the rest as a balance of saturated and monounsaturated fatty acids. Sucrose itself contributes to oxidative stress. The
10
most recent study showing that a lard-sucrose diet reduces BDNF levels found that additional vitamin E could normalize
these levels (3), suggesting that the diet reduces them by promoting oxidative stress and thus that it is the polyunsaturated
fat and sucrose in the diets rather than the saturated fat that are responsible for the problem.
A recent study purportedly showed that “saturated fat and cholesterol” impaired brain structure and memory in ma-
ture rats. The treatment diet was not only high in saturated fat and cholesterol but completely devoid of essential fatty
11
acids (EFA), which are necessary for brain function. Most of the calories came from casein, sucrose, and corn starch for
all the rats. Half of the rats were given 12 percent soybean oil and half were given 10 percent hydrogenated coconut oil
and 2 percent cholesterol. It has been known since 1960 that purified cholesterol at half this amount will accelerate the
onset of essential fatty acid deficiency and aggravate the resultant dermatitis and testicular degeneration, even though this
same amount of cholesterol does not raise the amount of essential fatty acids needed to cure the dermatitis and actually
enhances testicular development when essential fatty acids are present. The results of this study were most likely due
12
to essential fatty acid deficiency rather than saturated fat. In order to show a destructive effect of saturated fat itself, the
researchers should have provided the minimum EFA requirement in both diets.
REFERENCES
1. Lu J, Jiang C, Fontaine S, Thompson HJ. Ras may mediate mammary cancer promotion by high fat. Nutr Cancer. 1995;23(3):283-90.
2. DeWille JW, Waddell K, Steinmeyer C, Farmer SJ. Dietary fat promotes mammary tumorigenesis in MMTV/v-Ha-ras transgenic mice. Cancer Lett.
1993;69(1):59-66.
3. Slattery ML, Curtin K, Anderson K, Ma KN, Edwards S, Leppert M, Potter J, Schaffer D, Samowitz WS. Associations between dietary intake and
Ki-ras mutations in colon tumors: a population-based study. Cancer Res. 2000;60(24):6935-41.
4. Weijenberg MP, Lüchtenborg M, de Goij AF, et al. Dietary fat and risk of colon and rectal cancer with aberrant MLH1 expression, APC, or KRAS
genes. Cancer Causes Control. 2007;18(8):865-79.
5. Molteni R, Barnard RJ, Ying Z, Roberts CK, Gómez-Pinilla F. A high-fat, refined sugar diet reduces hippocampal brain-derived neurotrophic factor,
neuronal plasticity, and learning. Neuroscience. 2002;112(4):803-14.
6. Wu A, Molteni R, Ying Z, Gomez-Pinilla F. A saturated-fat diet garabatees the outcome of traumatic brain injury on hippocampal plasticity and
cognitive function by reducing brain-derived neurotrophic factor. Neuroscience. 2003;119(2):365-75.
7. Wu A, Ying Z, Gomez-Pinilla F. The interplay between oxidative stress and brain-derived neurotrophic factor modulates the outcome of a satu-
rated fat dieto n synaptic plasticity and cognition. Eur J Neurosci. 2004;19(7):1699-707.
8. Saito M, Kubo K. Relationship between tissue lipid peroxidation and peroxidizability index after alpha-linolenic, eicosapentaenoic, or docosa-
hexaenoic acid intake in rats. Br J Nutr. 2003;89(1):19-28.
9. Diniz YS, Cicogna AC, Padovani CR, Santana LS, FAine LA< Novelli EL. Diets rich in saturated and polyunsaturated fatty acids: metabolic shifting
in cardiac health. Nutrition. 2004;20(2):230-4.
10. Chaudhary DP, Boparai RK, Bansal DD. Implications of oxidative stress in high sucrose low magnesium diet fed rats. Eur J Nutr. 2007;46:383-
90.
11. Granholm AC, Bimonte-Nelson HA, Moore AB, Nelson ME, Freeman LR, Sambamurti K. Effects of a saturated fat and high cholesterol diet on
memory and hippocampal morphology in the middle-aged rat. J Alzheimers Dis. 2008;14(2):133-45.
12. Holman RT, Peifer JJ. Acceleration of Essential Fatty Acid Deficiency by Dietary Cholesterol. J Nutr. 1960;70(3):411-17.
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