Roland
That is very interesting. There is some evidence that omega 6 fats are
harmful in macular degeneration too, according to expert opinion (Prof P
Beaumont, Macular degeneration foundation Australia).

Another mechanism that is relevant to the interest of the list is glutamate
excitotoxicity. Dietary MSG is related to this.

Raito http://www.scientific-com.com/AJO/backissues/v1n2/article/ This paper
indicates that glutamate stimulates nerve cells to death (apoptosis to be
precise) in glaucoma, and that glaucoma patients have higher levels of
glutamate in the intraocular fluid (due to damaged retina). Thus a vicious
cycle is set up wherein the damaged retina becomes leaky and permits the
increased entry of glutamate from plasma. This glutamate then causes
apoptosis, thus exacerbating the visual loss. One would anticipate similar,
if not worse, leakiness in the diabetic eye.


While there is no mention of dietary MSG in Rait's paper, Blaylock documents
well that humans absorb MSG well (better than lab animals- I think around 7
times the elevation rats get on equivalent dosages) and it causes large
spikes in
serum glutamate level. It would be logical to see if dietary MSG restriction
could benefit patients with glaucoma and other eye diseases especially
macular degeneration. Drugs that block glutamate (eg memantine) slow down
cell loss from glaucoma and large trials are underway with this drug, but I
can't find any evidence of simple use of low MSG diets being used (please
let me know if they are).

Russell Blaylock's Excitotoxins makes it clear that MSG has undesirable
excitotoxic effects on nervous tissue, especially in
situations where the blood brain barrier is leaky or non-existent (eg
periventricular area, neurohypophysis, damaged retina & foetal brain)

http://news.bbc.co.uk/1/low/health/2352709.stm is a media article about
dietary MSG damaging the rat retina, and also implicating MSG in the high
level of normal tension glaucoma in Asian populations.

Pubmed has indexed a number of papers linking glutamate to cell loss in
glaucoma. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?CMD=Index&DB=PubMed

Ben Balzer



> -----Original Message-----
> From: Paleolithic Diet Symposium List
> [mailto:[log in to unmask]]On Behalf Of Roland Rohde
> Sent: Thursday, 26 February 2004 1:04 AM
> To: [log in to unmask]
> Subject: Omega-6 FAs and diabetic blindness
>
>
> Hi,
>
> I would like to direct the attention of the l
> ist members to a paper (1) that closes a crucial
> gap in our understanding of the sequence of metabolic
> events finally resulting in diabetic blindness.
>
> There is growing evidence that an accumulation
> of omega-6 fatty acids and especially their
> elevated blood levels (free fatty acids, FFAs)
> are causative factors in the development of
> endothelium dependent vascular diseases (1,2).
>
> The paper (1) convincingly shows that
> these FFAs in concentrations actually present
> in the blood of diabetics (literature in 1)
> and persons with a high cardiovascular risc (2)
> specifically induce the expression of certain
> endothelial surface molecules. The enhanced
> expression of these factors is a well known
> starting point for the attachment of blood cells
> ('leukocyte rolling') which are responsible for
> the induction and perpetuation (3) of
> inflammatory processes resulting in atheroslerosis.
>
> As FFAs are not only elevated in diabetes but in
> many high-risk states like obesity, stress, and
> insulin resistance, too, the omega-6 content
> of the adipose tissue could be responsible for
> the high blood levels as these fats are
> always primarily released.
>
> Diabetics are not only unable to keep their
> blood glucose levels low. The increase of the
> FFAs is often more severe and precedes the
> increase of glucose. Additionally, the
> diabetic liver is unable to extract and
> adequately metabolize omega-6 acids
> thus leading to high blood levels and
> consecutively to diabetic retinopathy and
> blindness (1).
>
> The actions of omega-6 FAs are in part dependent
> on their enzymatic conversion into hormonally
> active hydroxy acids (1). One receptor that is
> activated by these hormones (4) is the
> receptor for the thiazolidinedione class of
> antidiabetic drugs. A well known adverse effect
> of these drugs is weight gain. The increase of
> omega-6 consumption in westernized populations
> could to some extent be responsible for the
> obesity epidemic.
>
> Since about 100 years pathologists knew that the
> deposition of so called amyloid in pancreatic
> islets is typical for human, feline, and simian
> diabetes. Amyloid is an aggregation product of
> the hormone amylin which is stoichiometrically
> cosecreted with insulin. One of the best inducers
> of amyloid deposition are omega-6 FFAs (5,
> for Alzheimer-amyloid see 6).
>
> A very interesting reading in this context is the
> the paper of Staffan, Loren, et. al. (7),
> highlighting a principal difference between the
> nutrition in Kitava and Sweden. The intake of
> polyunsaturated omega-6 and monounsaturated fats
> in Kitava is very low (not more than 2% each
> compared to 16% mono and 5% poly in Sweden), while
> the intake of carbs is very high (70%). But
> vascular risk and body weight are both very low,
> in spite of low protein intakes.
>
> Such a diet is not very 'paleo' and points to the
> possible role of omega-6 uptake. It could even be
> more important than consumption of carbs.
>
> Omega-6 FAs disturb and interfere with delicate
> hormonal control systems (prostaglandins,
> leukotrienes, lipoxins, hydroxy-FAs, omega-3-FA
> interconversion) and are merely one enzymatic
> (lipogygenase-) step away from hormonally active
> substances.
>
> roland
>
> (1)
> Chen W, et. al.: Dyslipidemia, but not hyperglycemia,
> induces inflammatory adhesion molecules in human
> retinal vascular endothelial cells.
> Invest Ophthalmol Vis Sci. 2003 Nov;44(11):5016-22.
>
> (2)
> Yli-Jama P, et. al.: Serum free fatty acid
> pattern and risk of myocardial infarction:
> a case-control study.
> J Intern Med. 2002 Jan;251(1):19-28.
>
> (3)
> Ross R.: Atherosclerosis--an inflammatory disease.
> N Engl J Med. 1999 Jan 14;340(2):115-26.
>
> (4)
> Shankaranarayanan P, et. al.: IL-4 induces
> apoptosis in A549 lung adenocarcinoma cells:
> evidence for the pivotal role of
> 15-hydroxyeicosatetraenoic acid binding to
> activated peroxisome proliferator-activated
> receptor gamma transcription factor.
> J Immunol. 2003 Jan 15;170(2):887-94.
>
> (5)
> Ma Z, Westermark GT. et. al.: Effects of free
> fatty acid on polymerization of islet amyloid
> polypeptide (IAPP) in vitro and on amyloid fibril
> formation in cultivated isolated islets of
> transgenic mice overexpressing human IAPP.
> Mol Med. 2002 Dec;8(12):863-8.
>
> (6)
> Wilson DM, et. al.: Free fatty acids stimulate
> the polymerization of tau and amyloid beta peptides.
> In vitro evidence for a common effector of
> pathogenesis in Alzheimer's disease.
> Am J Pathol. 1997 Jun;150(6):2181-95.
>
> (7)
> Lindeberg S, et. al.: Determinants of serum
> triglycerides and high-density lipoprotein
> cholesterol in traditional Trobriand Islanders:
> the Kitava Study.
> Scand J Clin Lab Invest 2003;63(3):175-80.
>