Breast-feeding reduces SIDS:

or, does cow milk and infant formula cause it?

Links to citations of a new theory that toxic outgassing from fungi in the matress is a factor.
See the book: The Cot Death Coverup by Jim Sprott

Reducing the Incidence of Sudden Infant Death Syndrome
[South Med J 94(7):704-71, 2001. 2001 Southern Medical Association]

Excerpted from the article...

Sudden infant death syndrome (SIDS) is defined as the sudden and unexpected death of an apparently healthy infant. A thorough history and postmortem examination are typically insufficient to explain the cause of death. It is an affliction that has been recognized since biblical times.

Increasing the Breast-Feeding Rates

  Recent well-controlled studies have consistently shown that infants who were never breast-fed were two or three times more likely to die of SIDS than their breast-fed counterparts. Because of its high content of immunoglobulins and other antibacterial agents, breast milk has also been shown to have protective effects against illnesses such as rotavirus infections, ear infections, and upper and lower respiratory tract infections. It is not clear why breast-feeding is protective against SIDS. Gordon et al have speculated that the protective effect of breast milk could in part be attributable to the binding effects of IgA on bacterial toxins, such as staphylococcal enterotoxin C and Clostridium perfringens enterotoxin A, implicated in some cases of SIDS. Because breast-fed infants are usually healthier than their bottle-fed counterparts, they also tend to be resistant to whatever causes SIDS. Another possible explanation could be that, because of its richness in long-chain polyunsaturated fatty acids and other nutrients, breast milk enhances faster development of the central nervous system of the infants. Also, the frequent tactile stimulation of breast-feeding during the night may actually protect against SIDS.

  Nationally, about 60% of new mothers initiate breast-feeding, though only about 25% continue to do so 6 months after delivery. These figures vary widely depending on the region; they are highest in the Northeast and lowest in the Southeast. These rates are consistently lower among ethnic minorities than whites. In rural Mississippi, a recent survey showed that breast-feeding initiation rates were only 19% for blacks versus 44% for whites. Breast-feeding rates 6 months after delivery were not measured but were likely to have been substantially lower. Increasing the breast-feeding rates in the Delta region of Mississippi would necessitate educating and encouraging new mothers to breast-feed their infants.

  Breast-feeding education programs should preferably be initiated before delivery, and efforts should be continued after delivery. Some studies have shown that most breast-feeding counseling is done by allied health care workers. Physicians often report being inadequately prepared for the task during residency training. Physicians, nurses, nutritionists, and other health care professionals should therefore all be involved in such programs. For the programs to be effective, educational programs should involve not only mothers, but also husbands, friends, family members, and significant others. Other studies also show that social support systems, such as those at the workplace and in the hospitals, are necessary for a successful breast-feeding program.

Conclusion
Sudden infant death syndrome is the single most important cause of postneonatal mortality in the United States. In the Delta region of Mississippi, we recommend a three-pronged educational approach to reduce the incidence of SIDS in this region: (1) increasing the proportion of infants sleeping in the nonprone position, (2) decreasing the proportion of young infants exposed to passive smoke in homes, and (3) increasing the proportion of mothers initiating breast-feeding and continuing to breast-feed for at least 12 months after delivery. Until the cause of SIDS is found, our only hope of combating this endemic problem is through lasting changes in infant care practices in our community. Other factors, such as type of bedding, cosleeping, long QT syndrome, and ambient room temperature, may also be of some importance but, for now, too much emphasis on these may only add to parents' confusion. We believe that the three factors discussed in this paper are the most important, and health education programs focused on them will dramatically decrease the incidence of SIDS in this community.


J Hum Lact 1991 Jun;7(2):73-9
Comment in: J Hum Lact. 1991 Dec;7(4):175; discussion 176
Does breastfeeding protect against sudden infant death syndrome?
Bernshaw NJ.

  Sudden Infant Death Syndrome (SIDS), the leading cause of infant death from one to six months in the developed world, strikes approximately two infants per 1000 live births in the U.S. The characteristics of the infants who die suddenly and unexpectedly are non-specific; none are universal except for the age distribution. Therefore, an infant is recognized to have died from SIDS only after thorough examination fails to demonstrate any other cause for the death. It is the purpose of this paper to review the most populat hypotheses of the causes of SIDS and try to explain through published scientific findings how breastfed infants appear to be protected from this condition. Many hypotheses have been proposed to explain SIDS. Some deficiencies/problems are related to the infant, such as a defect in sleep and/or breathing control, severe infant botulism, infections, reactions to immunizations, hypersensitivity to cow's milk, "maternal deprivation syndrome." Other causes are attributed to maternal circumstances, such as lower socioeconomic status, prenatal health, smoking, and the winter season. Additional suggestions of potential causes of SIDS include baby's thiamine deficiency, and hormonal and/or biochemical imbalance. The occurrence of most of these circumstances can be associated with a lack of breastfeeding. Because SIDS occurs much less frequently in breastfed infants, it is speculated that breastfeeding protects infants against SIDS. However, scientific literature lacks uniformity in the definitions of breastfeeding (whether partial and exclusive). This specification is necessary to select control infants to elucidate the well documented substantial lower rate of incidence of SIDS in breastfed babies.

PMID: 2036158


Ann Ig 1989 Nov-Dec;1(6):1377-88
[Type of newborn infant feeding and an epidemiological approach to SIDS]. [Article in Italian]
Marinelli G, D'Innocenzo C, Marronaro MT.

  There are many etiopathogenetic theories that hypothesize several causes or factors supporting the onset of Sudden Infant Death Syndrome (SIDS). Among the SIDS factors there are bacterial endotoxins which can be conveyed into the organism in large amounts, by contaminated milk. An epidemiologic research was carried out on a sample of 258 mothers of children and boys attending some schools of L'Aquila district in 1988. It supplied data on the nursing procedures and about diseases with unknown aetiology related to nursing periods. The results obtained refer to the years 1974-84: 33.6% of sample was normal breast-fed infants. We found increasing percentage values referred to bottle-fed infants the first month of life (45% of sample in 1984); 22.5% of sample was bottle-fed infants only. Cows' milk was less and less used and it reached the 5% value in 1984. A case of hypothetic near-SIDS (0.4%) was found and another case which can be defined at SIDS-risk. It concerns two bottle-fed infants whose milk was diluted with simple drinking water. In addition a case of SIDS in a family was found: she was a girl aged 23 weeks who had begun drinking neat cows' milk only twenty days before the disease.

PMID: 2484473


Clin Allergy 1983 Jan;13(1):1-9
Latent anaphylactic sensitivity of infants to cow's milk proteins. Histamine release from blood basophils.
McLaughlan P, Coombs RR.

  Approximately 25% of infants tested released greater than 9% of their blood basophil histamine content in the presence of cow's milk proteins, indicating a degree or level of latent anaphylactic sensitivity to these allergens. Approximately 10% of infants show a considerably higher level of sensitivity (14-63% histamine release). These findings fulfil an essential tenet of the modified anaphylactic hypothesis for cot-death.

PMID: 6187497


Clin Exp Immunol 1976 Dec;26(3):542-8
The modified anaphylaxis hypothesis for cot death. Anaphylactic sensitization in guinea-pigs fed cow's milk.
Devey ME, Anderson KJ, Coombs RR, Henschel MJ, Coates ME.

  Guinea-pigs on a normal diet, but given cow's milk to drink instead of water, very soon became anaphylactically sensitive to cow's milk and may be fatally shocked following either i.v. injection or intratracheal inhalation of cow's milk.

PMID: 1009687


Med J Aust 1975 Dec 6;2(23):855-9
Sudden infant death syndrome in South Australia. Measurement of serum IgE antibodies to three common allergens.
Turner KJ, Baldo BA, Carter RF, Kerr HR.

  Radioallergosorbent test (RAST) studies showed that IgE antibodies to Dermatophagoides pteronyssinus (house dust mite), Aspergillus fumigatus and bovine beta-lactoglobulin were significantly elevated in the sera of infants who died as a result of the sudden death in infancy syndrome (SDIS). No significant differences were found in the levels of total IgE, IgA, IgG or IgM in the sera of SDIS victims or controls. The possible role of hypersensitivity in the aetiology of SDIS is discussed.

PMID: 768723


Dev Biol Stand 1975;29:208-16
RAST studies : IgE antibodies to Dermatogoides pteronyssinus (house dust mite), Aspergillus fumigatus and beta-lactoglobulin in sudden death in infancy syndrome (SDIS).
Turner KJ, Baldo BA, Hilton JM.

  The incidence of 2.5 SDIS cases per 1,000 live births found in Western Australia is in agreement with figures reported for other centres. While the age range of SDIS victims extended from two weeks to 15 months, 57 per cent of deaths occurred in children of two to four months of age. Boys outnumbered girls 1.6:1. Environmental factors are implicated in that the majority of deaths occurred in a biphasic distribution - autumn and late winter months. No significant differences were observed in total IgE levels in serum from SDIS victims, post mortem children who died in trauma of known aetiology and live control children of the same age range. Serum IgE antibodies to D.pteronyssinus were found in 37% of SDIS victims compared with 7% of matched controls (post mortem plus live groups). IgE antibodies to beta-lactoglobulin, the major allergen of cow's milk, appeared with twice the frequency in SDIS vs. control group but both groups showed a similar incidence of antibodies to the allergens of Aspergillus fumigatus. The prevalence of IgE antibodies to D.pteronyssinus in SDIS victims who died in the late winter -- early spring period was double that found in the group who died in the autumn period. Sixtyfour percent of the SDIS victims had antibodies to two or more of the three allergens tested while the control sera were positive to only one allergen. These results support the hypothesis that anaphylaxis induced by immediate hypersensitivity to D.pteronyssinus in particular may be one of the causative factors in SDIS in Western Australia.

PMID: 1097279

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