The information presented here can be confusing, but that is the nature of SIDS. The information I present on these pages is as complete as I could possibly make it and is the result of my reading and researching since my son died in April 1999. It took several months for me to compile all of the information I had into what you see here on the site. I personally do not agree with everything here, but my personal feelings have no place when it comes to information about SIDS. What's available on these pages is truly overwhelming, to have all this information and still not know why our babies continue to die for unknown reasons every single day. Please feel free to share a link to these pages but copying is strictly prohibited. It took a great deal of time and effort for me to pull all of this together, so please do not copy what I have worked so hard to complete. (c)Lydia Alves 2001, 2002

Theories on SIDS

Most researchers believe that babies who die of SIDS are born with one or more conditions that make them especially vulnerable to stresses that occur in the normal life of an infant, including both internal and external influences.

No one knows the fundamental cause or causes of SIDS. Doctors and researchers have learned that it isn't any one factor so much as a combination of factors. Some of these may include an anatomical defect in the brain, an abnormality in the immune system a metabolic disorder, or a heartbeat irregularity. The theory goes that when babies with any of these problems are faced with a challenge, they may be more likely to succumb to SIDS. For instance: sleeping on their stomach and breathing in too much carbon dioxide, or inhaling cigarette smoke or fighting a respiratory infection, or simply being overheated, any of these could trigger the death, while they are not solely the cause of the death.

Research has focused on such diverse causes as sleep apnea, arousal mechanisms, sleep-state organization, cardiac arrhythmias, thermoregulation abnormalities, occult viral infection, infant medications, sleeping position, allergy, metabolic disease, chronic hypoxia and autonomic instability. In the past many causes of SIDS have been postulated and have either remained unconfirmed or have been disproved. To date, no definite cause of SIDS has been determined.

We must continue to support scientists seeking solutions if we are to find any real answers to the perplexing puzzle of SIDS. Researchers believe that SIDS probably has more than one cause, although the final process appears to be similar in most cases. Research is difficult to perform because all of the subjects who should be in the control groups are deceased. It is important to realize that at the present time, SIDS can not be predicted, prevented or reversed.

Theories and Research

• Toxic Infection:
  This theory, presented in Milan in 2002, suggests that SIDS may be linked to infection with a common bacterium, stating that a shock-producing byproduct of E. coli was found in the blood of all SIDS babies they tested but in none of the infants they used as a comparison. This is the first time the specific E.coli protein has been implicated. The following is taken from the article dated April 25, 2002 by Emma Ross, AP Medical Writer.

  "Mainstream researchers have concentrated on respiratory obstruction as a possible mechanism, without any evidence that would support such a mode of death," said Dr. Paul Goldwater, who presented his study at the European Congress of Clinical Microbiology and Infectious Diseases in Milan.

  "Those researchers ignored autopsy findings that consistently show wet, heavy lungs in SIDS babies. This is never seen in cases of (suffocation)," said Goldwater, a researcher at the Women's and Children's Hospital in North Adelaide, Australia.

  Such a lung condition is often seen in cases of infection.

  Autopsies also consistently show small hemorrhages on the heart, lungs - which is rare in suffocation - and the blood of SIDS babies is unclotted, which is something never seen in suffocation cases, he added.

  Furthermore, he said, SIDS deaths captured on medical monitors have shown that these babies died of a shock-like process, Goldwater said.

  "The serum from babies who have died of SIDS (but not normal babies) is toxic to chick embryos and mice - indicating the presence of a toxin," he said.

  In his study, Goldwater tested the blood of 68 SIDS babies and 60 normal babies - some of whom had died of other causes and some of whom were alive - for infections that could explain autopsy findings in SIDS babies.

  He started with the common gut germ E. coli because varieties from SIDS cases are more often toxic to cells grown in a lab than are varieties found in healthy babies.

  Sometimes, E. coli bacteria (news - web sites) produce a protein called curlin, which scientists suspect may help the bacteria compete for a foothold in the competitive germ environment in the intestines, he noted.

  The bacteria themselves were found in the intestines of all the SIDS babies, but only in 80 percent of the healthy babies. However, curlin was detected in the bloodstream of all 68 of the SIDS babies but in none of the others, Goldwater said.

  "This indicated that curlin could be responsible for SIDS deaths, given the fact that curlin causes shock in laboratory mice," Goldwater said.

  There has already been some debate over the credibility of this theory. Many lean towards brain abnormalities as the cause of SIDS, yet some experts believe that such brain abnormalities may not be enough to cause death on their own. Some believe that this theory of toxic infection does not conflict with the popular brain-stem defect theory at all.

  For more information research Dr. Paul Goldwater who presented his study at the European Congress of Clinical Microbiology and Infectious Diseases in Milan, Italy.

• Toxic Gas:
  Due to the action of common household fungus on chemicals readily available in an infant's crib mattress, a highly toxic nerve gas is produced. This theory applies primarily to infants who are in a crib, although it could explain deaths of other infants who die in places other than a crib. This explanation for sudden infant death was realized in 1989 by British scientist Barry Richardson, first published in 1994. Compounds of the elements phosphorus, arsenic and antimony are very frequently present in bedding. In some instances they are added as part of the manufacturing process (e.g. for fire retardant or plasticising purposes). In other instances they occur naturally (e.g. in sheepskins, kapok and tree bark). Action of household fungus on these compounds can produce extremely toxic nerve gases. These are, respectively, phosphines from compounds of phosphorus, arsines from compounds of arsenic, and stibines from compounds of antimony. These gases shut down the central nervous system, resulting in cessation of heart and breathing function, and thereby causing cot death. The fungal generation of extremely toxic nerve gases from compounds of phosphorus, arsenic and antimony has been demonstrated many times over the last century. Some claim that the Limerick report disproved this theory, when in fact the Limerick report results supported the toxic gas theory. It was not a full investigation of the toxic gas theory, and in fact had some serious limitations. It did not investigate any mattresses other than those covered with PVC. They did not investigate natural products used as bedding, such as sheepskins. They focused only on stibine, which is only one of the three relevant gases. It's important to note that they were in fact able to generate this gas, thus proving the theory, however the report stated that while toxic gas was produced under laboratory conditions, no gas could be produced in a crib condition. Gas generation had already been achieved in crib conditions, failure by the Limerick Committee to do so does not negate that fact. Various researchers have found it difficult to achieve gas generation consistently using media with a neutral pH, but the pH of a baby's mattress is often higher, owing to the conversion of urea to ammonia. Experiments carried out using higher pH have achieved more consistent gas generation. In these tests fungus flourished and the amount of gas produced was greater than at neutral pH. According to this theory, an infant's sleeping environment must be protected from these harmful chemicals and gases. Jim Sprott, who had been suspicious of chemicals in a baby's environment for a long time, developed a cover that can be put on a baby's mattress which these deadly gases can not permeate. As an alternative to purchasing a cover, parents can purchase polythene sheeting or surgical rubber to make their own mattress wraps. If they select this option, the following instructions apply:
  
  
  • Use thick, clear (not coloured) polythene sheeting. The thickness of the polythene must be at least 125 microns.
  • On no account should PVC be used for wrapping mattresses.
  • If surgical rubber is used, it must be white or only lightly coloured. Surgical rubber can be used for mattress-wrapping only if it is known not to contain phosphorus, arsenic or antimony. This means that only very high grade surgical rubber is safe. Such rubber is expensive and difficult to obtain, although it may be available from hospital supply departments.
  • Place the polythene or rubber over the top of the mattress and down the ends and sides, and then secure it firmly beneath the mattress with strong adhesive tape.
  • The polythene or rubber should not be airtight on the underside of the mattress. Ventilation is needed in order to prevent condensation building up inside the polythene cover. This ventilation is perfectly safe, because the gases concerned are more dense than air. They fall away from the underside of the mattress towards the floor and therefore do not reach the baby. It must be airtight on the top and sides of the mattress. It is also imperative that the correct bedding is used with a polythene-covered or rubber-covered mattress.
  • On top of the polythene or rubber place a fleecy pure cotton underblanket and tuck this in securely. Then make the bed using only cotton or pure woolen blankets. Woolen blankets can contain phosphorus, but these blankets can be used as overblankets in a baby's crib because the bedding which is most likely to cause the gas generation concerned is underbedding because this is the bedding which becomes warm and moist, promoting fungal growth. Therefore woolen blankets are safe to use on top of a baby, but sheepskins, which are always placed underneath a baby, are not safe to use.

  Do not use any of the following items in your baby's crib:
  
  

  • Sheepskin
  • Any form of moisture-resistant cot mattress protector
  • Acrylic underblanket
  • Sleeping bag
  • Duvet

  If a mattress cover is purchased, it must be accompanied by a certificate of analysis showing that they contain no detectable phosphorus, arsenic or antimony (lower limit of detection 0.001% = 10mg/kg = 10ppm). Covering a baby's mattress will do no harm whatsoever, and even if one does not subscribe to this theory of toxic gases, covering a baby's mattress will also protect a baby from dust mites at the very least.

  For more information research Barry Richardson, Jim Sprott and his book The cot death : cover-up? ISBN Number 0140261982 or visit http://cotlife2000.com or http://www.criblife2000.com.

• Vitamin C Deficiency:
  Dr. Archie Kalokerinos and Dr. Glen Dettman, proved that severe depletion of a child's vitamin C level, precipitated by various insults including childhood vaccinations, could predispose a child to SIDS. It has been reported that when Aboriginal women and their babies' diets were supplemented with adequate vitamin C, a very high-risk group for SIDS, the results were that not a single baby died of SIDS in the nearly 8 years that the doctor was present in the community, and once that particular doctor was relocated, the infant deaths returned to the levels they had been previously. It is therefore suspected that SIDS is a reaction to acute infantile scurvy. This theory would also tie into the theory that SIDS is a problem in the heart's electrical system. The vitamin C deficiency theory is not inconsistent with that finding because vitamin C has a major affect on a healthy heart. It is entirely possible that adequate nutrition could lessen the effects of this heart problem to the extent that it is less often, or even rarely, fatal. One of the benefits of nutritional therapy is that it does not need to be chosen instead of any medical approach. It is instead, a necessary component of health.

  For more information research Archie Kalokerinos and his book Every Second Child. ISBN Number 0879832509.

• Brain Stem Defect:
  Growing evidence has shown that some babies who have died of SIDS have an abnormality or immaturity in the brain stem, which controls breathing and waking during sleep. Normally, babies can sense problems such as inadequate air or excessive carbon dioxide, but they might lack this protective mechanism if they have this brain irregularity.

• Triple Risk Model:
  SIDS is multifactorial, and many things have to occur at the same time and the body just shuts down. When three things happen simultaneously, it's called the triple risk model. SIDS can strike after certain things that would increase the likelihood of the triple risk model being set into motion have occurred. High risks would be vulnerability such as a defect in the brain stem and exogenous stressors (any external influences to the baby). The triple risk model requires three things to happen in order for SIDS to be the result. The baby must be in a critical development period, the child must be vulnerable, and there must be exogenous stressors. When these three things take place simultaneously, the result is SIDS. The first element of the model, the critical development period, encompasses rapid growth phases during the infant's first six months of life which may periodically destabilize the infant's system. During the developmental period, changes occur in homeostatic controls, such as sleeping and waking, breathing, heart rate, blood pressure and temperature. The second element, the vulnerable infant, represents an infant with an underlying defect or abnormality. In this model, normal babies do not die of SIDS; instead, there are pathophysiological reasons behind these seemingly sudden deaths, such as defects in regions of the brain that control respiration, heart rate, and during early life. The third element involves exogenous stressors, outside or environmental challenges which a normal baby can overcome and survive, that an already vulnerable baby night not. Stressors such as second-hand exposure to tobacco smoke, prone sleep position or an upper respiratory infection alone do not cause death for the infant, but may further tip the balance against an infant's chances of survival. According to this model, all three elements must come together for SIDS to result.

• Flaw in the Immune System:
  Research has shown that the immune system of some babies with SIDS generates a higher than normal number of white blood cells and proteins. Some of these proteins may interact with the brain to change heart rate and breathing during sleep, or put the baby into a deep sleep.

• Metabolic Disorder:
  Babies born with a certain metabolic disorder may be more vulnerable to SIDS. For example, if they lack one particular enzyme (medium chain acylCoA dehydrogenase), they may not be able to process fatty acids properly, and a buildup of these acids could trigger a rapid, fatal disruption in breathing and heart function. A medium chain acylCoA dehydrogenase deficiency prevents the infant from properly processing fatty acids. A build-up of these acid metabolites could eventually lead to a rapid and fatal disruption in breathing and heart functioning. If there is a family history of this disorder or childhood death of unknown cause, genetic screening of the parents by a blood test can determine if they are carriers of the disorder. If one or both parents is found to be a carrier, the baby can be tested soon after birth. Normally a baby is tested for only 6 metabolic disorders after birth. For more information please visit Save Babies Through Screening.

• Stress:
  Stress in a normal baby, caused by infection or another factor could play a role in SIDS. The number of cells and proteins generated by the immune system of some SIDS babies have been reported to be higher than normal. Some of these proteins can interact with the brain to alter heart rate and breathing during sleep, or can put the baby into a deep sleep. Such effects might be strong enough to cause the baby's death, particularly if the baby has an underlying brain defect.

• Nephron Deficiency:
  This kidney disorder has been linked to a number of infants who died of no known cause. Findings from this study still need to be evaluated.

• Nutrient Deficiencies:
  Certain nutrient deficiencies are the result of an inherited inability to properly absorb them from the diet, and can lead to various medical conditions. However, some conditions that appear as a nutrient deficiency are actually the result of an inability to produce the enzymes responsible for the use and location of nutrients upon digestion. It's possible that the genetic anticipation feature of some enzymes may play a role in SIDS, and that this potential risk could be avoided by supplementing a baby's formula with glutamine.

• Birth defect:
  Babies born with defects in other portions of the brain or body may also be more prone to a sudden death. Scientists believe that the abnormalities that are present at birth may not be sufficient to cause death. Other possibly important events occur after birth such as lack of oxygen, excessive carbon dioxide intake, overheating or an infection. For example, many babies experience a lack of oxygen and excessive carbon dioxide levels when they have respiratory infections that hamper breathing, or they rebreathe exhaled air trapped in underlying bedding when they sleep on their stomachs. Normally infants sense such inadequate air intake, and the brain triggers the babies to wake from sleep and cry, and changes their heartbeat or breathing patterns to compensate for the insufficient oxygen and excess carbon dioxide

• Abnormalities in the Brain:
  Some research suggest that abnormalities in the area of the brain responsible for controlling breathing and arousal during sleep may prevent some babies from sensing a lack of oxygen or too much carbon dioxide. Normally these conditions would cause an infant to wake or cry, allowing breathing to return to normal. Researchers suspect that these brain abnormalities may be related to exposure to toxic substances, or to cigarette smoking during pregnancy, or it may be a result of a lack of a vital compound in the prenatal environment, such as sufficient oxygen. Cigarette smoking during pregnancy, for example, can reduce the number of oxygen the fetus receives.

• Carbon Dioxide Rebreathing:
  Some theorize that when a baby rebreathes exhaled carbon dioxide rich air that it puts a baby at risk of SIDS. This theory believes that many SIDS deaths can be avoided simply by making sure that the baby always has access to fresh air, including using a fan to help circulate the air around a baby. This theory claims that the danger period is primarily between 2 and 4 months of age, stating further that for the first two months of a baby's life they don't sleep long enough to reach a dangerous condition. After four months a baby is much larger and more animated during sleep. It claims that a five month old baby has grown out of the danger zone, but does acknowledge that SIDS occurs in babies who are older.

• Ammonia:
  Two decades ago a book claimed that ammonia gas produced from the urine on wet diapers in babies in is the cause of SIDS. It was rejected by the medical profession, but according to some, the theory was never discredited. In fact ammonia has never been the subject of any medical published study. This theory says that ammonia produced from urine on wet diapers is a lethal toxic poison which is dangerous even for adults at only 50 parts per million. Ammonia is also responsible for upsetting the delicately balanced carbon dioxide, oxygen uptake mechanism by causing airway obstruction. Ammonia could potentially be in a baby's crib due to the inherent instability of urea that's excreted in urine, and is readily converted into ammonia through bacterial action. It has a pungent odor and is severely irritating to the membranes in the nose, throat and lungs, and it is possible for it to be absorbed into the bloodstream. Ammonia acts principally on the upper respiratory tract, and has a more corrosive action on tissue than most acids. Ammonia can cause death in a variety of ways, the most common is pulmonary oedema. In relation to SIDS, ammonia inhalation affects each step of respiration. Chronic hypoxemia symptoms and chronic underventilation are the two most common SIDS autopsy features that defy explanation. Some believe that this explanation regarding ammonia is the basic cause of SIDS.

  For more information please research James W. Tyler and his book Sudden Infant Death Syndrome: Probable causes and Simple Prevention. ISBN Number 0806963468

• Abnormalities in Brain Receptors:
  One study provides further support for the theory that abnormalities in brain receptors responsible for controlling breathing may play an important role in SIDS. Researchers studied 79 infants who died from SIDS or other causes and found significant differences between the two groups in the ability of a neurotransmitter called kainate to bind to a receptor in a particular region of the brain stem. Neurotransmitters are chemical messengers that help relay signals between cells. Scientists speculate that such binding problems may disrupt communication between nerve cells, preventing infants from responding when they are getting too much carbon dioxide or not enough oxygen. Earlier research on SIDS infants found abnormalities in another receptor of the same brain region, the arcuate nucleus. The arcuate nucleus is a portion of the brain that is likely to be involved in controlling breathing and waking during sleep. A baby with a flawed arcuate nucleus might lack a protective mechanism which would wake them, and as a result they succumb to SIDS. Such a scenario might explain why babies who sleep on their stomachs are more susceptible to SIDS, and why a disproportionately large number of SIDS babies have been reported to have respiratory infections prior to their deaths. Infections as a trigger for SIDS may explain why more cases occur during the colder months of the year, when respiratory and intestinal infections are more common.

• Failure to develop:
  In support of the developmental imbalance hypothesis, there are observations by several investigators of decreased heart rate variability during NREM sleep in ALTE victims and in the siblings of SIDS victims. A similar decrease in heart in heart rate variability has been observed in patients who are at high risk of sudden cardiac death following myocardian infarction, usually due to the blocking of a coronary artery.

• Cell defect:
  A cell defect was discovered in one small area of the brain stem of SIDS victims by pathologist Dr. Hannah Kinney. She theorizes that the defect keeps infants from noticing high levels of carbon dioxide. Infants sometimes inhale carbon dioxide in air caught between their blankets. A healthy infant reacts to high levels of carbon dioxide by waking up to cough and free the airway. SIDS infants apparently do not possess the internal carbon dioxide detector and inhale fatal levels. Autopsies showed the defect in a significant number of infants who died of SIDS. Autopsies of infants who died of other causes did not reveal any sign of such a defect. Although the defect may be a factor of SIDS, it is not necessarily the only cause.

• Development
  A Critical period when all babies are more vulnerable, such as a time of rapid growth.

• Sleep-induced Arrhythmia:
  This is a loss of rhythm in the heart, and may be a factor of SIDS. It has been hypothesized that changes in autonomic nervous system activity during sleep could precipitate an arrhythmia resulting in sudden death. Some potential abnormalities of autonomic function that might initiate a cardiac arrhythmia and SIDS have been reviewed and it is possible that excess vagal tone (refers to the vagal nerve) that might occur during episodes of apnea could lead to profound bradycardia and asytole. A developmental imbalance of the autonomic nervous system could lead to the destruction, neutralization or change in polarity and repolarization with the myocardium. Changes in the autonomic tone that occur during sleep could precipitate life-threatening cardiac arrhythmias in infants through several mechanisms, however at this point in time their role in SIDS is unknown.

• QT Interval:
  This is a measure of ventricular repolarization, which is the process in which the membrane, after depolarization, is polarized again with the myocardium, with positive charges on the outer and negative charges on the inner surface. The QT interval occurs in normal infants between 2 and 4 months of age. Although ventricular tachy-arrhythmia associated with prolongation of the QT interval has been proposed as a potential mechanism of SIDS, significant prolongation of the QT interval has not been documented in 100 infants following ALTE.

• Apparent Life Threatening Event (ALTE):
  Significant bradycardia or sinus arrest was observed in 6% of the infants in one study following an ALTE. In the vast majority of these subjects the arrhythmias observed during sleep were secondary to apnea and hypoventilation. Another possible mechanism of sudden cardiac death in SIDS victims is ventricular tachycardia (VF), secondary to increased sympathetic nervous system activity during REM sleep. Against this hypothesis is the absence of any documented abnormalities of the myocardium or conduction system in victims of SIDS. In addition, ventricular arrhythmias have been infrequently observed in infants following an episode of ALTE.

A variety of causes, rather than one single factor, probably accounts for most SIDS cases.

In trying to find a cause and cure, scientists are exploring the development and function of the nervous system, the brain, breathing and sleeping patterns, body chemical balances, autopsy findings and environmental factors. There is cause for hope. SIDS deaths have decreased dramatically since the advisory that babies sleep only on their backs to sleep.

Although research into SIDS continues, researchers warn that SIDS is still not fully understood, and information to date has not provided a cure or a risk-screening test. While recent breakthroughs may not provide all the answers, these theories are worthy of continued research.

Remember - Information provided here is for general purposes only. Only your physician can provide specific diagnoses and advice tailored to your family's needs.