Big fat problems with American infant formulas

by Dr. Joseph Debé

“You want the very best for your baby.” So states a printed advertisement for one of the leading American infant formulas. Unfortunately, the sorry truth is that “the very best” is not available in the United States. The problem is that American infant formulas do not contain docosahexaenoic acid (DHA) or arachidonic acid (AA), which are normally present in breast milk.

So what are DHA and AA, and why are they important? DHA and AA are what are referred to as long chain fatty acids. DHA and AA are constituents of fats and lipids. As structural components within cell and subcellular membranes, DHA and AA are vital to normal human physiology by influencing membrane “traffic”. They also serve as precursors to messenger molecules, which regulate diverse physiologic functions such as immune function and muscle contraction.

The brain is composed largely of fats, and DHA is normally the most abundant fatty acid within brain tissue. AA is the second most plentiful fatty acid in the brain. DHA is also highly concentrated in the retina of the eye. The brain does most of its developing during gestation and the first several years of life. When DHA is lacking in the diet (formula), other fatty acids are used to occupy its place within cell membranes. These include docosapentaenoic acid in full term infants and Mead and dihomo Mead acid in preterm infants. What’s important here is that when DHA is not supplied in infant formula it is replaced within the brain by other fatty acids. Animal studies have found that replacement of DHA by docosapentaenoic acid produces abnormal functioning of the membranes, altered enzyme function, reduced cellular energy production and altered learning behavior. (1)

Cell membrane fatty acids influence the binding and, therefore, the function of hormones and other biological messenger molecules. DHA and AA influence neurotransmitter levels and their binding to cell receptors. DHA deficiency results in reduced levels and receptor binding of dopamine. This produces altered states of attention, motivation and reaction to stimuli and reward. Decreased dopamine levels are seen in ADHD (Attention Deficit Hyperactivity Disorder). Not surprisingly, DHA and AA insufficiency are common in ADHD. DHA deficiency may also contribute to nervousness, irritability, hostility, aggression, memory loss, depression, Alzheimer’s disease, schizophrenia, lower IQ, non-insulin dependent diabetes, obesity, hypertension, cardiovascular disease, and poor visual function.

At least some infant formula companies take the position that supplying alpha-linolenic acid and linoleic acid, the precursors of DHA and AA respectively, is sufficient since infants can convert these into DHA and AA. (2) The fact is that although the body has enzymes that can manufacture DHA and AA from these other fatty acids, this ability is very limited in infants and cannot meet their requirements. (3) Numerous studies have compared the red blood cell fatty acid profiles of breast-fed and formula-fed infants and have found significantly lower levels of DHA and AA in the formula-fed infants, regardless of varying the concentration of alpha-linolenic and linoleic acids. (4,5,6,7,8,9,10) On the other hand, supplementation of infant formulas with DHA and AA results in red blood cell fatty acid profiles extremely similar to those of breast-fed infants. (7, 8, 9, 10) It is important to supplement with both DHA and AA, as providing one but not the other produces a state of imbalance. (7,11)

Red blood cell fatty acid levels are a good reflection of levels within the brain and, indeed, breast-fed infants have been found to have significantly more DHA within brain tissue than formula–fed infants. (12) Newborns start off with a supply of DHA within their tissues, provided the mother had adequate DHA status during pregnancy. If supplied with a dietary source, the brain continues to incorporate DHA and AA for several years after birth. Stored DHA is quickly depleted in the newborn. This situation is especially problematic for premature infants because the brain and the retina do a lot of developing during the last trimester of pregnancy. Premature birth interferes with this development. A premature infant fed a diet devoid of preformed DHA and AA will become deficient more quickly than will a full term infant.

Compared to formula feeding, breastfeeding has been found to produce long-lasting improvements in cognitive ability and educational achievement. (13) Data analysis has determined that DHA and AA content of breast milk is at least partly responsible for this difference. One study found an IQ advantage of preterm infants fed breast milk by tube compared to a formula-fed group (14), indicating an effect beyond the actual act of breastfeeding. There have also been several studies that have compared regular infant formula to formula supplemented with DHA and AA as to effect on mental development. These studies have found infants receiving DHA and AA-enriched formula to have greater cognitive ability than infants fed unsupplemented formula.(15,16)

Studies have also been done to examine the effect of dietary DHA and AA on visual function. A recent one-year study measured the red blood cell fatty acid composition and visual function of 108 infants over 52 weeks time. Twenty-nine of the infants were breast-fed and the rest were fed either plain infant formula or formula supplemented with DHA and/or AA. It was found that the fatty acid make-up and visual function were similar between the breast-fed and fatty acid supplemented groups but were inferior in the unsupplemented formula group.(9) Another similar study measured visual acuity in breast-fed, formula-fed, and DHA supplemented formula-fed infants at 16 and 30 weeks of age. It was found that the infants in the unsupplemented formula group had poorer visual function than the other two groups. Red blood cell fatty acid levels of DHA correlated with visual acuity in all infants at both ages tested. Interestingly, infants breast-fed for less than sixteen weeks had poorer visual acuity than infants receiving a steady supply of DHA did, whether from breast milk or supplemented formula. (11)

The foregoing information would seem to indicate the wisdom of adding DHA and AA to infant formulas. This is the official recommendation of several organizations including the British Nutrition Foundation, the International Society for the Study of Fatty Acids and Lipids, and the United Nations Food and Agriculture Organization and World Health Organization joint expert committee on fats and oils in human nutrition. DHA and AA- enriched infant formulas are available in fifty countries, but the United States is not one of them. You can buy DHA-AA enriched food for your kitten or puppy, but the FDA has not approved DHA and AA for addition to human infant formulas!

Breast-feeding will always be best. However, if infant formula is going to be used, it should contain DHA and AA. These formulas can be purchased in other countries. One such formula is called Materna Premium Stage 1 by Maarbarot, an Israeli company. A second option is to add DHA and AA to American infant formula. DHA supplements are sold in health food stores. It is important to not supplement with EPA, another fatty acid that accompanies DHA in fish oil, as this can result in lower tissue levels of arachidonic acid. A good source of pure DHA is algal oil. The brand I recommend is Martek. Arachidonic acid is quite a bit more difficult to find but may be attainable.

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10.Clandinin MT, Van Aerde JE, Parrott A, Field CJ, Euler AR, Lien E. Assessment of feeding different amounts of arachidonic and docosahexaenoic acids in preterm infant formulas on the fatty acid content of lipoprotein lipids. Acta Pediatr 1999;88:890-6.

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15.Willatts P, Forsyth JS, DiModugno MK, Varma S, Colvin M. Effect of long-chain polyunsaturated fatty acids in infant formula on problem solving at 10 months of age. Lancet 1998 Aug 29;352(9129):688-91.

16.Carlson SE, Werkman SH, Peeples JM, Wilson WM. Long-chain fatty acids and early visual and cognitive development of preterm infants. Eur J Clin Nutr 1994 Aug;48 Suppl 2:S27-30.