First off, a h/t to Verity Jones who pointed me at two interesting articles about sulphate / sulfate metabolism.
They give an overview of the importance of sulphate to metabolism and the epigenetic influence it may have, plus look at using Epsom Salts as an easy way to get sulphate and the benefits it may bring.
That eventually lead to some “digging around” that resulted in finding this particularly interesting article:
Download PDF here:
A fairly technical paper that goes into the full Monty of genetics, epigenetics, metabolic pathways, the works. It ties together, in oh so genteel and circumspect a way, the elusive impacts of environmental insults such as vaccination, heavy metal exposure, Bis-Phenol-A, and even some high fructose corn syrup and sunscreen use. All leading back to a common metabolic function (sulphates) and the myriad impacts it can have.
I’m going to quote some of the more attainable bits here, but the whole paper is worth the read (at least if you have some genetics and biochem background). I’ve bolded bits of particular interest.
Entropy 2012, 14(10), 1953-1977; doi:10.3390/e14101953
Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?
Samantha Hartzell and Stephanie Seneff* email
Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge 02139, MA, USA
* Author to whom correspondence should be addressed.
Received: 28 September 2012; in revised form: 16 October 2012 / Accepted: 16 October 2012 / Published: 18 October 2012
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Abstract: Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the alarming rise in the incidence of autism in the last three decades suggests that environmental factors play a key role as well. This dichotomy can be easily explained if we invoke a heritable epigenetic effect as the primary factor. Researchers are just beginning to realize the huge significance of epigenetic effects taking place during gestation in influencing the phenotypical expression. Here, we propose the novel hypothesis that sulfates deficiency in both the mother and the child, brought on mainly by excess exposure to environmental toxins and inadequate sunlight exposure to the skin, leads to widespread hypomethylation in the fetal brain with devastating consequences. We show that many seemingly disparate observations regarding serum markers, neuronal pathologies, and nutritional deficiencies associated with autism can be integrated to support our hypothesis.
Keywords: autism; epigenetics; cholesterol sulfate; DNA methylation; sulfotransferases; heparan sulfate; folate; cobalamin; zinc
Folks from MIT are usually pretty good about getting things figured out right. They manage to integrate many disparate observations into a coherent whole package at the level of enzyme systems and biochemistry.
While many different markers have been observed to be abnormal in association with autism, reduced levels of plasma sulfate and subsequent reduced sulfation capacity are among the most consistent findings in autism research . A recent interest in sulfated glycosaminoglycans (GAGS) has spurred investigations highlighting the importance of sulfate in the developing brain . It is proposed here that sulfate depletion, caused by a combination of various environmental factors and genetic predispositions, is an important contributor to the development of ASD, and that epigenetics plays an important role in readjusting the phenotypical expression to cope with a sulfate deficiency.
The idea that impaired sulfate metabolism is a key factor in autism is not new [5–7]. An excellent review chapter  discusses several abnormal factors related to sulfate chemistry that have been found in association with autism. Observed serum imbalances include low plasma levels of free sulfate, abnormally high ratios of plasma cysteine to sulfate, and high loss of sulfite, sulfate and thiosulfate through the kidneys, as well as reduced levels of urinary thiocyanate . Additionally, many sulfatedependent neurodevelopmental processes have been found to be defective in association with autism.
The sulfate pathways matter, it shows up in lab tests, the developmental pattern of the brain is changed with low sulfate levels, and it is related both to the mother and child level of sulphate as there is an epigenetic component to the process.
In the remainder of this paper, we will first discuss the importance of sulfation in biology. We will then look specifically at the role of sulfate in the developing brain, focusing on serotonin and the glycosaminoglycans. We next turn our attention towards evidence of abnormal sulfate metablism in association with autism, including impaired sulfoconjugation capacity and increased sulfate excretion. We will then discuss available theories concerning possible causes of this impairment, including genetic effects and environmental effects. In particular, we will emphasize the effect of insufficient sunlight exposure to the skin and will argue that this issue goes beyond vitamin D3 deficiency. We further discuss how other known characteristics of children on the autism spectrum, such as gastrointestinal problems, increased androgen levels, and increased inflammation, can be explained by the sulfate deficit, and we will show that treatments aimed at repairing sulfate metabolism have shown some benefit. Finally, we will discuss the evidence for an epigenetic effect related to genomic hypomethylation in the fetus in association with autism. We conclude with a discussion section where we elaborate on our hypothesis and demonstrate how it can explain all of the complex factors associated with autism. Finally, we discuss simple lifestyle changes that could be implemented to address the problem.
That “addressing the problem” is mostly about eliminating the development of new cases, only a little bit about small improvements in present cases.
Of particular interest to me was the sun connection. Sunlight does more than just make Vitamin D. It also forms cholesterol sulphate and make sulphate available to the body. Or recent life style habits of hiding indoors and being covered in clothes or slather on sunscreen may well be partly causal in a sulfate deficit and some of the resulting risk of autism.
I’m skipping over a lot of the evidence and specific discussions of metabolic pathways and biochem. For that, read the article. Mostly I’m quoting bits with interesting observations and conclusions in them.
Sulfate is a vital nutrient required for proper development, and as such, normally flows in abundant supply from the mother to the fetus. The developing child receives sulfate from the mother through the placental villi and later through colostrum, the mother’s first milk . Especially during the third trimester, renal reabsorption of inorganic sulfate increases in the mother, increasing serum sulfate levels. This causes an increase in inorganic sulfate concentrations in the mother’s amniotic fluid and an enrichment of cholesterol sulfate in the placental villi. It has been hypothesized that sulfation of cholesterol, making it amphiphilic, allows it to penetrate the placental barrier . It also then becomes a potential source of sulfate to the fetus. Cholesterol sulfate levels in the villi rise dramatically throughout pregnancy. The concentration of cholesterol sulfate increases from 3.93 to 18.35 to 23.75 pmol/mg dry mass over the course of the three trimesters, a six-fold increase from the first trimester to the third trimester . During this same period, serum inorganic sulfate in the fetus is even higher than serum inorganic sulfate in the mother .
Within the brain, sulfate transporters are expressed most strongly in the cerebellum and the hippocampus, implying that these two regions carry out important processes requiring sulfate regulation . Interestingly, both of these brain regions have been implicated in the pathogenesis of autism
There is a huge rise in suphate demand in the developing child and the mother provides that if available. So staying out of the sun, slathering on sunscreen, not eating sulphur rich foods (i.e. the present fad of avoiding meats, eggs, cheeses, etc.) all challenge this need for extra sulfate. The result may well be epigenetic changes if sulfate is low.
Of special interest is a recent discovery that a postnatally induced heparan sulfate deficiency in the brain is capable of causing autistic behavior in mice, including impairments in social interaction, expression of stereotyped, repetitive behavior, and impairments in ultrasonic vocalization, all without causing detectable changes in cellular arrangement in the brain .
They’ve done it in mice.
Consistent with the idea that excess levels of serotonin are involved in the pathogenesis of autism is the fact that prenatal cocaine exposure, which increases serotonin, is heavily associated with autism at a rate of 11.4% . A strong connection exists between autism and Smith-Lemli-Opitz Syndrome (SLOS), which is caused by a defect in the enzyme catalyzing the last step in cholesterol synthesis. Fifty three of those with SLOS develop autism , which might also be explained through serotonin, as cholesterol depletion has been shown to cause a loss of serotonin transporter (SERT) activity .
Don’t do coke, and you need cholesterol, so being on hyper low cholesterol diets might not be a bright idea.
There are two routes for the metabolism of homocysteine in the body, the first of which leads to methionine through the methionine synthase reaction, and the second of which leads to cystathionine, catalyzed by cystathionine beta synthase (see Figure 1). The methionine synthase route enables methylation, while the cystathionine route protects from oxidation. Thus, low methionine levels will lead to reduced methylation and low cysathionine levels will lead to increased oxidative stress. Due to the fact that the methionine synthase reaction relies on B12, folate, and the reduced folate carrier, a lack of any one of these components will ultimately impair methylation. Zinc deficiency may also play a role.
You need your vitamins and minerals. Especially B12, folate, and zinc. Genetic defects in their metabolism may also be a problem (that was in the next paragraph that I left out. ;-)
This suggests that the consequence of less effective methionine metabolism might be more relevant during the period when the fetus is developing in utero. Given that hyperhomocysteinemia, along with reduced levels of B12 and folate, is associated with obesity , this might help to explain the association between obesity in the mother and autism risk in the child .
Along with folate, cobalamin is also a critical cofactor in the methionine synthase reaction. One protein of interest in this process is transcobalamin II (TCN2), the transport protein which mediates the cellular uptake of B12 . In this case, the TCN2776GG variant, which has a decreased binding affinity for B12, reduces its cellular uptake. This allele was found to increase the risk of autism 1.7-fold . Indeed, it has been observed that B12 deficiency is associated with developmental regression that in many ways parallels the observed pathology associated with autism .
Cobalamin too. If prone to obesity, this might indicate a genetic problem with those vitamin pathways so special care is in order.
hydrolyzes homocysteine thiolactone , thus participating in its conversion to sulfate . An association between reduced PON1 activity and autism in the United States was reported in . Factors which might have contributed to this deficiency that were considered included excess dietary high fructose corn syrup (HFCS), insufficient dietary magnesium, and exposure to mercury. An association between PON1 deficiency and HFCS exposure has been confirmed in rats .
Overall, low methionine levels are observed in many children diagnosed with autism. As oxidative stress reduces methionine synthase activity , a combination of genetically impaired folate transport, B12 transport, and oxidative stress might work in tandem to produce this outcome.
Rats fed high fructose corn syrup have their enzymes (PON1) shift in the same direction as that seen in autism and in a way that interferes with sulphate metabolism. Exposure to oxidative stress and mercury not helpful (and can be contributory) and keep your magnesium levels good too.
In short get some sun and avoid the crap foods and HFCS laden sodas and crap packaged junk foods. Keep toxin exposure down.
Certain genetic tendencies related to the uptake of folate and B12 increase the risk of autism substantially, but they do not act alone. It has been found that three genetic risk factors for autism: variants in catechol-O-methyl transferase (COMT), methyl tetrahydrofolate reductase (MTHFR), and cystathionine beta synthase (CBS) act in tandem with vitamin depletion to increase autism risk . This is an especially important issue for the many Americans who do not meet the RDA of these vitamins.
Increased use of sunscreen and decreased exposure to the sun may also play a role in the development of autism. One possible mechanism is through vitamin D, which appears to regulate the sodium-sulfate cotransporter NaSi-1. Mice lacking the vitamin D receptor (VDR) had NaSi-1 expression in the kidney which was reduced by 72%, causing urinary sulfate excretion to increase by 42% and serum sulfate concentration to decrease by 50%.
Individual genetics play into enhanced risks, so some folks need to be more careful than others. If an at risk type (relatives with issues or family history) be especially careful with nutrition levels.
Mice models demonstrate that the sun induced sulfate and Vit-D is important since knocking out the receptor for Vit-D caused a lot of sulfate dumping from the kidneys. Get your sun, don’t be over using sunscreen. (And think about adopting a mouse ;-)
In  and , we proposed that sunlight exposure to the skin is essential not only for vitamin D3 synthesis, but also for the synthesis of sulfate in the skin, and subsequently its combination with cholesterol to form cholesterol sulfate. The skin synthesizes an abundance of cholesterol sulfate, and it has been proposed that the skin is the major supplier of this nutrient to the tissues . In fact, many sunscreens contain a form of retinoic acid (vitamin A) which is a known inhibitor of cholesterol sulfate synthesis by squamous cells in the epidermis . Cholesterol sulfate supply would likely be severely impaired in SLOS–over half of SLOS children are diagnosed with autism, and it is likely that impaired synthesis of cholesterol sulfate in the skin leads to impaired sulfate supply throughout the body. We propose that a similar impairment in the supply of cholesterol sulfate due to the impaired sunlight stimulated synthesis of sulfate in the skin may be implicated in many other cases of autism.
There is a known defect that causes some autism by impairment of cholesterol sulphate, so it is highly likely that other impairment of cholesterol sulphate formation could also cause autism. Sunshine is good. Cholesterol is good.
In fact, there are several epidemiological clues that sunlight exposure in the mother, proposed here to protect against sulfate deficiency, is preventative of autism in the child. Pregnancies which occur in northern latitudes and births timed so that the third trimester corresponds with the late winter or early spring months are more likely to produce a child with autism . In Nordic countries, mothers from foreign backgrounds, who often have darker skin, wear more conservative clothing, and consume reduced amounts of protective foods such as meat and fish, are more likely to have children with autism .
Especially in the third trimester when sulfate demand is highest in the fetus, get your sun or use a UV “Lizard Lamp” of the kind prescribed for Seasonal Affective Disorder. Avoid wearing a burka. Get out there in the sun and show some skin. Enjoy your meat and fish.
Another increasingly common condition associated with a vitamin D deficiency  is diabetes, which has recently been shown to be the most important prenatal maternal risk factor for the development of autism . Interestingly, vitamin D3 in the mother is also a risk factor for the development of preeclampsia , which, in turn, is also a strong risk factor for future autism in the fetus .
I just have to wonder how much of the “Diabetes Epidemic” is due to sucking down quarts of high fructose corn syrup and sitting inside way from the sun, or covering up in paranoia with excess clothes and sunscreen when going anywhere near outdoors…
In those individuals already compromised by a reduced sulfation capacity, postnatal administration of acetaminophen (branded as androsten, paracetamol or tylenol) could be partially responsible for the rise in autism. Acetaminophen is a xenobiotic which is neutralized and metabolized by the body largely through sulfation, and administration of acetaminophen to rats has been shown to dramatically reduce sulfation capacity to the point of saturation . In fact, acetaminophen use following the measles-mumps-rubella (MMR) vaccine in children has been shown to increase the subsequent risk for autism, and particularly for regressive autism .
Shoving Tylenol into your kid at every cry or red spot is a bad idea. Not only does acetaminophen risk blowing out the liver of adults; it screws up your sulfate metabolism and coupled with the stress of a vaccination could be a Very Bad Idea for infants.
As I recall it, our pediatrician was fond of pushing Tylenol at the kids for any discomfort, and offered it after our MMR vaccine and we declined (partly due to my “paranoia” about it… that is looking ever more justified…)
Methionine synthase (MS) activity has been shown to be significantly susceptible to deactivation by numerous environmental toxins . Both heavy metals and the ethylmercury-containing vaccine preservative thimerosol potently interfere with MS activation and impair folate-dependent methylation. Further, it has been demonstrated clinically that elevated mercury body-burden in subjects diagnosed with autism was associated with transsulfuration abnormalities, likely arising from increased oxidative stress and decreased detoxification capacity .
In a multi factor causality, you don’t want to be adding factors. Heavy metals, like mercury, are another factor. So thimerosol alone may not be a problem, and vaccination alone may not be a problem and Tylenol alone may not be a problem, and low cholesterol sulphate from sunscreen use may not be a problem, but stack them all up you can have a problem… So just say no to each of them. Then put back in the vaccinations on a schedule that does not increase risks.
Each is shown to have a contributory effect to the sulfate availability suppression. Removing each will help get normal sulfate.
Depleted cysteine stores, as in the case of autism, stress both sulfate and glutathione synthesis, since both processes compete for cysteine. As expected, this leads to low levels of glutathione (GSH) in autism. Low GSH results in an increase in inflammation, microglial activation, neuro inflammation, and expression of nitric oxide (NO) through inducible nitric oxide synthase (iNOS), all pathologies found in autism [100–102].
In addition to the ‘gut’ effects (leaky gut, various sensitivities) it looks like low sulfate can also cause excess inflammation. Along with other effects. I wonder to what extent getting sulfate levels up can help with generic inflammation related diseases. Get some sun, soak in a mineral bath, suck down a mineral water, and have a bit of BBQ. See if that arthritis lets up…
I found this next bit particularly encouraging. While not a cure, it can be helpful:
7. Increasing Sulfate Levels Can Help Alleviate Autistic Symptoms
Although much of the pathology associated with autism seems, unfortunately, to be related to brain development during the critical period and is irreversible, an increase in sulfate levels has, in fact, been shown to alleviate symptoms in some children diagnosed with autism. In one study, a reduction in urinary sulfate excretion achieved through supplementation with molybdenum, an essential metal catalyst in sulphite oxidase, correlated with improvement in autistic symptoms in patients . Oral and transdermal glutathione supplementation, administered to children on the ASD spectrum, led to significant increases in plasma reduced glutathione, sulfate, cysteine, and taurine . In the case of autism, which is hard to pin to one definite cause, it is becoming clearer that many different pathologies lead to the sulfate deficiency which in turn contributes to neurological damage.
Depending on the root cause of the sulfate deficiency, different dietary supplements may be beneficial in treating autism. These include, specifically, the vitamins and minerals involved in the transsulfuration pathway (Figure 1): B12, B6, folate, magnesium and zinc. While several of these nutrients have been proposed for the alleviation of autism, findings have been generally inconsistent [104,105]. It is likely that the dysfunctional intestinal epithelium impairs uptake of these nutrients .
So getting the sulfate levels up can be helpful. I’m surprised they didn’t mention the direct absorption via a bath in Epsom Salts or just taking a bit of Epsom Salts in water. Dasani Water, IIRC, has MgSO4 in it. Correcting specific vitamins and minerals can also be helpful.
The article then goes on into a discussion of epigenetics that is quite interesting, and the potential that low sulfate in the mother may lead to epigenetic changes in the child to adapt to low sulfate availability (via methods that cause other problems…). So it is important for Mom to get some sun, not suck down too much HFCS, and have good sulfate levels.
DNA methylation is the first layer of epigenetic effects, and environmental toxins negatively impact DNA methylation globally . Maternal supplementation of folate, particularly in the month before gestation and the first two months of pregnancy, has been demonstrated to have a strong protective effect against autism in the fetus. This could be directly attributed to the important role that folate plays in the methylation pathway. However, one has to be cognizant of the effect that folate will have in redirecting methionine towards methylation pathways rather than towards sulfation pathways, thereby introducing further strain on the sulfation system under conditions of sulfur deprivation.
Keeping maternal folate levels up is important, but increases the need to keep maternal sulfate levels high as it creates a competition between two pathways that can show up in epigenetic methylation changes.
The paper then goes on for quite a while admiring the particular genetic / epigenetic changes observed in various rodents and people and drawing the connections… It gets a bit thick then, but here is an example.
We have previously proposed that endothelial nitric oxide synthase (eNOS) is a moonlighting enzyme whose main product is sulfate, catalyzed by sun exposure, and, further, that the sulfate is combined with cholesterol to produce cholesterol sulfate in the skin, which is then transported to all the tissues. The enzyme’s physical structure suggests that cobalamin may facilitate the reaction, as it fits snugly into the heme pocket of NOS isoforms, and is known to inhibit nitric oxide synthesis . eNOS switches to nitric oxide (and hence nitrate) synthesis following calcium entry, calmodulin binding and phosphorylation , which we view as a pathological response. eNOS is membranebound in caveolae in its so-called “inactive” state, and caveolin suppresses nitric oxide synthesis. Nitrate can substitute for sulfate for ionic buffering in the blood, but the resulting global sulfate deficiency has pathological consequences . Indeed, autism is associated with excess nitrite and nitrate in the blood [128,129]. We hypothesize that the 1,047 genes that were upregulated and the 444 genes that were downregulated as a consequence of hypomethylation during embryogenesis  have to do with adjusting system-level parameters to account for severe sulfate deficiencies.
The basic idea being that you can shift to a nitrate buffer instead of a sulfate buffer in emergencies, but it has costs. So you can still have a viable child during conditions of severe sulfate shortage, but not an ideal one. So better to avoid those epigenetic gene regulatory changes and keep the sulfate levels proper to begin with.
Specific experiments involving the agouti mice are compelling and supportive of our hypothesis. In , it was demonstrated that prenatal exposure to the estrogenic environmental toxin, bisphenol A (BPA), induced non-specific gene hypomethylation, leading to favored expression of the yellow phenotype. However, concurrent supplementation with folate, cobalamin, betaine and choline, important nutrients for the supply of methyl groups, abolished this effect.
Again with the mice… poor dears… but this time demonstrating an epigenetic impact on them from Bisphenol-A causing hypomethyltion (a bad thing). But enough vitamins and supplements could prevent it. Lending some credence to the Bisphenol-A as yet another cofactor / partial factor. So best to just avoid it in plastic baby bottles and plastic soda bottles and plastic can liners and…
And folks wonder why I like to eat food that is not packaged in plastic nor heated in plastic…
And then there is this bit. A rather complex interaction of the mother taking added folate, but being low on sulfate, leading to a worse result. I wonder how many mothers were taking their added folate, but avoiding the sun and using a lot of sunscreen… and on a low cholesterol diet.
While folate deficiency is recognized as a risk factor in autism, folate supplementation has met with varied success . Interestingly, these authors propose that there may be a specific relationship between regressive autism and poor response to folate therapy. Furthermore, others have found an autoimmune reaction to folate in the central nervous system in association with autism, which prevents its transport across the blood brain barrier, even when levels are sufficient in the blood stream, associated with the so-called cerebral folate deficiency (CFD) syndrome . In a study of 93 children with autism, over 75% were found to have CFD syndrome, and 44% of the parents who were tested also had the condition.
We hypothesize that all of these observations can be explained if we envision a scenario where the mother is supplemented with folate during gestation, but is severely deficient in supplying cholesterol sulfate to the fetus. The folate will redirect methionine towards methylation pathways rather than sulfotransferase pathways, thus further depleting the already dangerously low sulfate levels. However, the bioavailability of methyl groups will result in a false sense of security, whereby hypermethylated DNA sets up a phenotype that anticipates sulfate sufficiency. It is only after birth and continued subjection to factors that further deplete sulfate, such as lack of sun exposure and toxic environmental chemicals, that the autoimmune reaction to folate develops to spare methionine for its urgent need as a source of sulfate in the brain.
Their ‘wrap up’ reads to some extent like a list of things to do that doctors have been telling folks NOT to do for the last few decades… Gee, I wonder…
If our hypothesis is correct, then there is some optimism that reversing the epidemic would not be difficult. If people can be made aware of the importance of sun exposure to the skin to health, then they can alter their lifestyle habits to spend additional time outdoors without sunscreen. Dietary changes involving increases in foods that are good sources of sulfur, such as animal-based proteins and cruciferous vegetables, will help to assure an adequate supply of sulfur, the substrate for sulfate synthesis. Foods that are rich in choline, betaine, folate, cobalamin and zinc would also be encouraged, as these nutrients play an important role in the methylation and sulfotransferase pathways. People should also be encouraged to consume cholesterol-rich foods, as this lessens the burden for cholesterol synthesis, and will likely increase the bioavailability of cholesterol sulfate. Finally, people should make a conscious effort to minimize exposure to xenobioics, which deplete sulfate supplies. Whether the damage can be repaired in individuals already on the autism spectrum is doubtful, but enrichment along these lines would surely be of benefit to them as well.
Xenobiotics is a “polite” way of saying “foreign chemicals” like Bisphenol-A, Tylenol, and all that laundry list of chemical soup on most processed packaged foods…
So avoid the chemical soup. Get some sun on bare skin without sunscreen. Eat your cholesterol rich foods like eggs, sea food, and meats. Animal foods. Oh, and your cabbages and kales and turnips.. you know, all those ‘stinky vegetables’ that trendy folks like to avoid…
For completeness, here is the conclusion entire:
In this paper, we have presented the novel hypothesis that there is a strong link between DNA hypomethylation and sulfate deficiency, both of which have been proposed as key factors associated with autism spectrum disorder. Methionine sits as the crossroads of the methylation and transsulfuration pathways, and thus a deficiency in methionine supply impacts both systems. We hypothesize that insufficient sun exposure to the skin compromises the supply of cholesterol sulfate both to the fetus and to the infant postnatally, and that the concurrent exposure to environmental toxins further depletes sulfate and sulfur metabolites. We further hypothesize that hypomethylation during gestation implements a switch towards the production of nitrate rather than sulfate for ionic buffering in the blood stream, and that this has huge negative consequences due to the critical need for sulfate in neuronal maturation. Confirmation of the hypothesis awaits further studies. If our hypothesis is correct, then increased dietary sulfur and increased sun exposure for both the mother and the infant should be strongly encouraged, along with avoidance of exposure to sulfate-depleting environmental toxins.
“Methionine” is found in meats… So we have here a statement to eat some meat, do it in the sun, avoid the chemical crap, keep your cholesterol intake at a good level, and make sure you have a good sulfate intake. (My preference would be some time in the mineral bath and drinking mineral water, but YMMV.)
In other words, ignore the advice to slather on loads of sunscreen. Don’t be paranoid about sun exposure. Tell the folks nagging you about meat and eggs and cholesterol to go stuff it, and treat yourself so some well deserved time at the spa. Be a bit of a hedonist and enjoy life and the rich foods it offers. Kind of the exact opposite of some of the paranoid self flagellatory advice from the “usual suspects”… Oh, and toss the chemical factory foods and keep you and the kid off of Tylenol and away from plastic packaging with Bisphenol-A and similar substances. Have real foods, prepared at home from whole ingredients and in a natural setting. Roast a chicken, or mash some potatoes, and put butter on them. It’s Fine.
That’s what this is saying to me. But as I could be wrong, please read the whole paper yourself. You might well pick up something I’ve missed or gotten wrong. Me? I’m going to go have a ham and cheese omelet for breakfast… with buttered toast on home made bread. Washed down with a bit of sulfate rich mineral water and coffee.