Re: oxalates and strep/

[Guest guest]

Gayle,

You and I are a bit on the same page here, because there keep being people on

our listserve for oxalate who think that strep may " come out " during dumping.

One reason this " might " happen is if the bacteria gets encased in oxalate during

an infection, because oxalate was high at the time. It IS known that bacteria

can survive in that encased environment and can multiply again once released.

Some bacteria and plants have a way of switching their metabolism to survive

lack of food using the glyoxylate cycle, which is an abbreviated TCA cycle.

Here is the TCA cycle:

http://employees.csbsju.edu/hjakubowski/classes/ch112/pathways-charts/tca1detail\

..gif

Here is the glyoxylate cycle:

http://www.chembio.uoguelph.ca/educmat/chm452/gif/glycycle.gif

The difference between the two cycles is that at isocitrate, an enzyme called

isocitrate lyase makes glyoxylate, which can then be converted to malate, to

catch back up to the rest of the TCA cycle at about " nine o'clock " .

Unfortunately, if malate synthase is weak, that glyoxylate could also be

metabolized to oxalate.

In plants, this cycle might purposefully make oxalate to release to the soil in

order to bring more minerals up to the plant for absorption, but probably more

of a plant's oxalate comes from metabolizing ascorbic acid. A plant can't go

out shopping, so it has to be clever in how to get its nutrition to come to it!

Oxalate is also kept in plants in specialized cells called idioblasts that we

don't have which keeps the plant oxalate from being toxic to the plant.

A long time ago scientists stated as fact that humans didn't have this cycle,

but nobody had looked! We actually have this glyoxylate cycle in ourselves,

though very little study has been done in humans. It is used in a STRESS

response, like during infection, like maybe even in a strep infection?

When people keep complex carbohydrates low, this cycle may be employed trying to

get energy when the way to get energy is more restricted. Years ago, I proposed

this to DAN! as an explanation for why SCD if it induces this cycle may step up

malate synthase enough to help detoxify some glyoxylate in people where this

enzyme is strong. If malate synthase is NOT stepped up, but isocitrate lyase

IS, then it would instead lead to INCREASED oxalate. Maybe this is why

sometimes when children are sick with autism, their " autism " is better!

It is so important to know the complexity of things before offering simple

interpretations of mechanisms. Usually, nothing about biology is simple. After

sixteen years studying all this, I can say that with authority!

But if or when that cycle is invoked, then some people may be able to have a

strong malate synthase activity and maybe that makes SCD work for them. We just

don't know, but NOBODY needs to be pretending that kids with autism all have the

same biochemical issues. They don't!

But getting back to strep, according to pubmed, NOBODY has studied any

streptococcus species for this glyoxylate cycle! But here it is in a database

for streptococcus pyogenes:

http://www.genome.jp/kegg-bin/show_organism?menu_type=pathway_modules & org=soz

If strep uses this cycle when it " comes out " and is under attack by the immune

system, then it may generate additional oxalate that would add to the body

burden and that may cause the similarity of symptoms of a strep-sourced oxalate

with dietary sourced oxalate. Some kids may have both!

NOBODY has also studied WHERE the oxalate comes from when it is detoxing from

the body, except that scientists have looked at biopsy samples in oxalate

damaged organs years after a liver transplant has solved the problem in genetic

(primary) hyperoxaluria. As they detoxify, blood and urine levels of oxalate

RISE!

What might be evidence that this has happened?

I found out in the last two days that there are sensors in cells for

intracellular crystals that will turn ON interleukin-1. This cytokine's

nickname is pyrogen because it is responsible for fever. A child I've heard

about on facebook had strep this past week and a fever that was high for four

days, I think. The fever is gone now, but now the child is sleeping 16 hours a

day. IL-1 can induce this sort of problem with sleep and it happened to my

daughter after a fever she had three years ago and it lasted a week.

One of the problems is that when you are sick, you generally slow down eating

(he did), so your total oxalate load goes down, and you might end up with a

" dump " at the same time as the infection, further increasing the circulation of

oxalate!

There is so much about oxalate that people in the autism community have never

heard because there was too much pressure from various leadership NOT to support

a " third " diet, except suggesting it as a " third option " after the others didn't

work that could be used for a proposed " small subgroup " . Nobody tried to define

that subgroup because there was really no way to say who DIDN'T have an oxalate

problem!

I regret that these sorts of " strategic " decisions didn't help get kids well

from oxalate issues or get the information to you earlier!

There is no time like the present!

Trying_Low_Oxalates .

Med Hypotheses. 2008 Aug;71(2):222-8. Epub 2008 Apr 29.

Visceral adipose tissue specific persistence of Mycobacterium tuberculosis may

be reason for the metabolic syndrome.

Erol A.

Namik Kemal University, Faculty of Medicine, Department of Internal Medicine,

Namik Kemal Caddesi 14, Tekirdag, Turkey. adnanerol@...

Abstract

Mycobacterium tuberculosis (Mtb) is highly successful intracellular pathogen.

Infection is maintained in spite of acquired immunity and resists eradication by

antimicrobials. Following bacillaemia, small numbers of bacteria are

disseminated to the extrapulmonary organs most likely including visceral adipose

tissue by a mechanism that may involve the migration of M. tuberculosis within

dendritic cells. In this lipid rich environment, Mtb can metabolize the fatty

acids in a glyoxylate cycle dependent manner, and a state of chronic persistence

may ensue. The persistent bacilli primarily use fatty acids as their carbon

source. Expression of isocitrate lyase (ICL), gating enzyme of glyoxylate cycle,

is upregulated during infection. ICL is important for survival during the

persistent phase of infection. Expression of adipokines, particularly monocyte

chemoattractant protein-1 (MCP-1), which is a potent proinflammatory cytokine,

may be increased. MCP-1 contributes both to the recruitment of macrophages to

adipose tissue and to the development of insulin resistance in humans. In

addition, prolonged low level immune stimulation induces local adipolipogenesis,

increasing visceral fat. Increased delivery of free fatty acid to the liver may

stimulate the glyoxylate cycle-induced gluconeogenesis, raising hepatic glucose

output. Hence, inhibition of the triggering enzyme ICL, which initiates all the

pathologies related to persistent Mtb infection, may block the growth of the

bacteria and may resolve the systemic metabolic complications.

PMID: 18448263

> >

> > So how do you know when you should avoid high oxalates?

> >

> > I strongly suspect I should avoid it with my younger guy. But the older, I

> > don't know.

> > I hate to cut out stuff like carrots and spinach because there's so much

> >benefit

> >

> > to them. Vitamin C has been a God-send. We rely on peanut butter too, not

only

> >

> > to mix in supps but as a source of protein because beef came back elevated

so I

> >

> > try to watch it. I hate to take these things away if oxolates are not an

issue

>

> > for him.

> >

> > what signs should I be watching for?

> >

> > -Tammy

> >

>