Saturday, June 24, 2006
Diabetic Peripheral 2
Diabetic Peripheral Neuropathy and Acrylamide - 2
See previous “Diabetic Peripheral Neuropathy and Acrylamide” in
http://andreswhy.blogspot.com
Dated 21/06/200
Major Money-making Opportunity.
“The end-product is path-dependant “ … AW
“You are what you eat.”
“Personalized Eating”
There are only two ways to measure the content of food :
Lacking such a device , a monoclonal antibody strip should recognize the presence and concentration of a simple chemical like acrylamide . This should be easy to make .
A personalised smart eating utensil would advise the eater of nutritional needs and no-no’s via something like blue-tooth.
This can be done now with present technology .
Market : initially , about 10% of population :huge
This is a killer app!
A personal note:
I suffered increasingly for 14 years with peripheral diabetic neuropathy . When I became aware of the arguments below , I immediately (on 12/06/2006) cut out any food prepared at over 120 degrees Celsius .
The effect was dramatic. Within 2 days , a lot of the symptoms had disappeared .
( The curve is a standard exponential decreasing with time .) After 5 days I could sleep without chemical help . It is now day 10 . Glucose levels have improved , and instead of feeling hypo , I feel hungry . Still , early days .
I take daily 4x3x3 grams of Evening Primrose Oil (since 12/06/2006) , since this is the only clinically proven way of repairing peripheral neuropathy damage . Feeling is slowly returning to my feet and toes . Interestingly , there is no side-effect like in recovering from frostbite . (Tingling and burning sensations have disappeared . I still have occasional restless feet .)
The worst-case half-life of acrylamide is 8 days .
So 3-4 months should bring levels really low as long as no new acrylamide is ingested
The feeling that you have found something that actually works is indescribable .
Not only-knees up , Mother Brown , but feet-up as well !
Andre
1. Background:
1. Acrylamide (ACR) is a potent neuro-toxin . See http://epa.gov.iris/subst/0286.htm
2. It induces neural damage both in the Central Nervous System (CNS) and the Peripheral Nervous System (PNS) even at sub-chronic levels .
This has important implications for diabetes , alzheimers , etc
To quote from the experimental results in the link below :
“Thus, subchronic exposure to ACR affected the expression of death-related proteins in the CNS and PNS tissue, which indicate there is the early molecular regulatory mechanism of apoptosis in the neuropathy induced by ACR.”
Note that according to this experimental result , the CNS is somehow buffered against low continual dosages of acrylamide , but not the PNS .
The effect of acrylamide seems to change the expression of genes bcl-2 , bax and caspase-3 to bring about apoptosis of the Scwann-cells in the myelin sheath . The result is a train crash in the axon transport system of the PNS long before effects are noted in the CNS .
Indeed , the buffering might be seen as an evolutionary work-in-progress since the invention of the use of fire + metal ( = frying) .
You might say that rats (used in the experiments) are not fire-using , but that is not correct . They do certainly eat cooked discards from human sources , and have done so for at least a million years . Given their proven speed of adaptation to poisons , propensity for gene-swapping and short gestation period , they are almost certainly more adept at handling acrylamide poisoning than humans . This seems to be an opportunity for some nifty forced accelerated rat-evolution and gene-science .
Since these are epigenetic expressions , the evolution can be very fast . It might even be amenable to outside intervention in humans .
The problem is that the buffering system in the CNS is probably a stupid thing like increasing the rate of myelin-cell production . If you reduce the acrylamide by eating healthier , over-production of myelin-sheaths leads to things like Alzheimers . Eating too much acrylamide leads to neuropathy and (probably) diabetes . This is easily testable by feeding rats with Alzheimers acrylamide in controlled dosages . Has this been done ?
See link :
http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3048&uid=16242231&db=pubmed&url=http://linkinghub.elsevier.com/retrieve/pii/S0300-483X(05)00385-9
2. Acrylamide formation.
“The end-product is path-dependant “ … AW
The standard theory of formation of acrylamides involves a temperature over 120 degrees Celsius somewhere in the process .
So it was a shock when the FDA found very high concentrations of acrylamide in canned black olives and bottled prune juice . At first glance , the temperatures of canning and bottling (127 – 140 celsius) does not seem to high enough .
But it seems that both are washed in lye . And in the US the lye is laced by up to 0.2% of acrylamide ( see FDA regulations below) .
(It was extraordinarily difficult to get any information about processes and intermediate materials , mainly because the present model is path-independent . Potent sub-chronic intermediate chemicals are not taken into account at all .)
Black Ripe Canned Olives:Most olives in California are grown to supply canneries with green fruit to produce this canned dark olive we see on pizzas and in tacos and in every grocery store. The dark color is not a result of ripeness but of a process of lye curing and oxidizing the olive. The cured olive is pasteurized and canned in a light salt brine. If you open one of these cans and a small film is floating on top of the brine, it is most likely oil from the olive that has floated to the top. Many cans of olives are needlessly thrown out for this reason.
FDA regulations .
These were formulated before the extent of acrylamide became known . Due to bureaucratic inertia , they have not changed . So some foods are still prepared using dangerous levels of acrylamide .
AA=AcrylAmide
PAA=PolyAcrylAmide
U.S FDA (1998) regulates AA as an indirect food additive, a component of food-contact surfaces for single and repeated use. PAA has been approved for various applications. MPC in food contact PAA solutions: 0.02% (1990); MPC for PAA food additive: 0.05 to 0.2%.
US FDA has established regulations for use of AA: It can be used (l) in washing or to assist in the peeling of fruits and vegetables using lye if the concentration does not exceed 10 mg/l in the wash water and if no more than 0.2% AA is present; (2) in adhesives as a component (monomer) of articles intended for use in packaging, transporting, or holding food in accordance with the conditions prescribed in 21 CFR part 175.105; as (3) a component (monomer) of the uncoated or coated food-contact surface of paper and paperboard intended for use in producing, manufacturing, packaging, processing, preparing, treating, packing, transporting, or holding dry food in accordance with the conditions prescribed in 21 CFR part 176.180; (4) as a monomer in the manufacture of semirigid and rigid acrylic and modified acrylic plastics in the manufacture of articles intended for use in contact with food in accordance with the conditions prescribed in 21 CFR part 177.1010. (5) AA-sodium acrylate resins can be used as boiler water additives in the preparation of articles that will be in contact with food, if the water contains not more than 0.05% by weight of AA; (6) PAA can be used as a film former in the imprinting of soft-shell gelatin capsules if no more than 0.2% of the monomer is present; (7) homopolymers and copolymers of AA may be safely used as food packaging adhesives, providing the amount used does not exceed that "reasonably required to accomplish the intended effect"; (8) AA-acrylic acid resins may be safely used as components in the production of paper or paperboard used for packaging food, providing the resin contains less than 0.2% residual monomer and that the resin does not exceed 2.0% by weight of the paper or paperboard
From another site : an interesting snippet for rats :
From PMID: 2539170 [PubMed - indexed for MEDLINE]
Quote :
“This study supports the concept that acrylamide neuropathy worsens with moderate intensity of running activities for a prolonged period and that recovery may occur if vigorous exercise is avoided.”
Another feather in the scale of acrylamide vs hyperglucose : vigorous exercise will decrease glucose faster than acrylamide.
3. This is a simple , but very clear experiment illustrating the links between acrylamide and diabetes .
The implications of this article are enormous . Is it true ? Has any other comparable experiments been done ?
The inference is that , taken together with the sub-chronic data about acrylamide , the chicken-and-egg situation between acrylamide and diabetes resolves to a “acrylamide first” picture .
In other words , the diabetic feedback condition is kicked off by prolonged sub-chronic acrylamide poisoning . While acrylamide does not accumulate in tissue or blood , the damage it does is repaired at a slower rate than ingestion . Diabetes seems to be an attempt of the body to get nutrients to nerve-extremities that have been cut off from supplies by axon-transport diminishment .
Instead of a disease , diabetes (at least at the start ) seems to be an attempt at a cure .
Curing it :
1.Cut all acrylamide ingestion . This means any food prepared at over 120 degrees Celsius or containing very small amounts ( micrograms ) of acrylamides (like canned olives , bottled prune juice , anything washed by lye)
2. Do not exercise vigorously until 8 days have passed since cutting all acrylamide ingestion .
3. Type II diabetes should taper off . (This needs to be proven.)
4. Take high concentrations of Evening Primrose Oil: the only clinically proven substance to reverse peripheral neuropathy . Obviously , it will only work well if intake of acrylamide is sharply reduced .
Attenuation of acrylamide-induced neurotoxicity in diabetic rats.Al Deeb S, Al Moutaery K, Arshaduddin M, Biary N, Tariq M.Neuroscience Research Group, Armed Forces Hospital, P.O. Box 7897 (W-912), Riyadh, Saudi Arabia.In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weighing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in group 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days/week) for 2 weeks. The rats in group 3 and 4 were made diabetic by administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant (p 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.PMID: 10758354 [PubMed - indexed for MEDLINE]
Happy eating
Andre
See previous “Diabetic Peripheral Neuropathy and Acrylamide” in
http://andreswhy.blogspot.com
Dated 21/06/200
Major Money-making Opportunity.
“The end-product is path-dependant “ … AW
“You are what you eat.”
“Personalized Eating”
There are only two ways to measure the content of food :
- Find it directly by measuring it right before you eat it . A smart fork , spoon or knife . Smart false teeth ( a new meaning for spittoon) .
Lacking such a device , a monoclonal antibody strip should recognize the presence and concentration of a simple chemical like acrylamide . This should be easy to make .
A personalised smart eating utensil would advise the eater of nutritional needs and no-no’s via something like blue-tooth.
This can be done now with present technology .
Market : initially , about 10% of population :huge
This is a killer app!
- Trace the path of preparation . This is laborious , and practically impossible in a complex society .
A personal note:
I suffered increasingly for 14 years with peripheral diabetic neuropathy . When I became aware of the arguments below , I immediately (on 12/06/2006) cut out any food prepared at over 120 degrees Celsius .
The effect was dramatic. Within 2 days , a lot of the symptoms had disappeared .
( The curve is a standard exponential decreasing with time .) After 5 days I could sleep without chemical help . It is now day 10 . Glucose levels have improved , and instead of feeling hypo , I feel hungry . Still , early days .
I take daily 4x3x3 grams of Evening Primrose Oil (since 12/06/2006) , since this is the only clinically proven way of repairing peripheral neuropathy damage . Feeling is slowly returning to my feet and toes . Interestingly , there is no side-effect like in recovering from frostbite . (Tingling and burning sensations have disappeared . I still have occasional restless feet .)
The worst-case half-life of acrylamide is 8 days .
So 3-4 months should bring levels really low as long as no new acrylamide is ingested
The feeling that you have found something that actually works is indescribable .
Not only-knees up , Mother Brown , but feet-up as well !
Andre
1. Background:
1. Acrylamide (ACR) is a potent neuro-toxin . See http://epa.gov.iris/subst/0286.htm
2. It induces neural damage both in the Central Nervous System (CNS) and the Peripheral Nervous System (PNS) even at sub-chronic levels .
This has important implications for diabetes , alzheimers , etc
To quote from the experimental results in the link below :
“Thus, subchronic exposure to ACR affected the expression of death-related proteins in the CNS and PNS tissue, which indicate there is the early molecular regulatory mechanism of apoptosis in the neuropathy induced by ACR.”
Note that according to this experimental result , the CNS is somehow buffered against low continual dosages of acrylamide , but not the PNS .
The effect of acrylamide seems to change the expression of genes bcl-2 , bax and caspase-3 to bring about apoptosis of the Scwann-cells in the myelin sheath . The result is a train crash in the axon transport system of the PNS long before effects are noted in the CNS .
Indeed , the buffering might be seen as an evolutionary work-in-progress since the invention of the use of fire + metal ( = frying) .
You might say that rats (used in the experiments) are not fire-using , but that is not correct . They do certainly eat cooked discards from human sources , and have done so for at least a million years . Given their proven speed of adaptation to poisons , propensity for gene-swapping and short gestation period , they are almost certainly more adept at handling acrylamide poisoning than humans . This seems to be an opportunity for some nifty forced accelerated rat-evolution and gene-science .
Since these are epigenetic expressions , the evolution can be very fast . It might even be amenable to outside intervention in humans .
The problem is that the buffering system in the CNS is probably a stupid thing like increasing the rate of myelin-cell production . If you reduce the acrylamide by eating healthier , over-production of myelin-sheaths leads to things like Alzheimers . Eating too much acrylamide leads to neuropathy and (probably) diabetes . This is easily testable by feeding rats with Alzheimers acrylamide in controlled dosages . Has this been done ?
See link :
http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3048&uid=16242231&db=pubmed&url=http://linkinghub.elsevier.com/retrieve/pii/S0300-483X(05)00385-9
2. Acrylamide formation.
“The end-product is path-dependant “ … AW
The standard theory of formation of acrylamides involves a temperature over 120 degrees Celsius somewhere in the process .
So it was a shock when the FDA found very high concentrations of acrylamide in canned black olives and bottled prune juice . At first glance , the temperatures of canning and bottling (127 – 140 celsius) does not seem to high enough .
But it seems that both are washed in lye . And in the US the lye is laced by up to 0.2% of acrylamide ( see FDA regulations below) .
(It was extraordinarily difficult to get any information about processes and intermediate materials , mainly because the present model is path-independent . Potent sub-chronic intermediate chemicals are not taken into account at all .)
Black Ripe Canned Olives:Most olives in California are grown to supply canneries with green fruit to produce this canned dark olive we see on pizzas and in tacos and in every grocery store. The dark color is not a result of ripeness but of a process of lye curing and oxidizing the olive. The cured olive is pasteurized and canned in a light salt brine. If you open one of these cans and a small film is floating on top of the brine, it is most likely oil from the olive that has floated to the top. Many cans of olives are needlessly thrown out for this reason.
FDA regulations .
These were formulated before the extent of acrylamide became known . Due to bureaucratic inertia , they have not changed . So some foods are still prepared using dangerous levels of acrylamide .
AA=AcrylAmide
PAA=PolyAcrylAmide
U.S FDA (1998) regulates AA as an indirect food additive, a component of food-contact surfaces for single and repeated use. PAA has been approved for various applications. MPC in food contact PAA solutions: 0.02% (1990); MPC for PAA food additive: 0.05 to 0.2%.
US FDA has established regulations for use of AA: It can be used (l) in washing or to assist in the peeling of fruits and vegetables using lye if the concentration does not exceed 10 mg/l in the wash water and if no more than 0.2% AA is present; (2) in adhesives as a component (monomer) of articles intended for use in packaging, transporting, or holding food in accordance with the conditions prescribed in 21 CFR part 175.105; as (3) a component (monomer) of the uncoated or coated food-contact surface of paper and paperboard intended for use in producing, manufacturing, packaging, processing, preparing, treating, packing, transporting, or holding dry food in accordance with the conditions prescribed in 21 CFR part 176.180; (4) as a monomer in the manufacture of semirigid and rigid acrylic and modified acrylic plastics in the manufacture of articles intended for use in contact with food in accordance with the conditions prescribed in 21 CFR part 177.1010. (5) AA-sodium acrylate resins can be used as boiler water additives in the preparation of articles that will be in contact with food, if the water contains not more than 0.05% by weight of AA; (6) PAA can be used as a film former in the imprinting of soft-shell gelatin capsules if no more than 0.2% of the monomer is present; (7) homopolymers and copolymers of AA may be safely used as food packaging adhesives, providing the amount used does not exceed that "reasonably required to accomplish the intended effect"; (8) AA-acrylic acid resins may be safely used as components in the production of paper or paperboard used for packaging food, providing the resin contains less than 0.2% residual monomer and that the resin does not exceed 2.0% by weight of the paper or paperboard
From another site : an interesting snippet for rats :
From PMID: 2539170 [PubMed - indexed for MEDLINE]
Quote :
“This study supports the concept that acrylamide neuropathy worsens with moderate intensity of running activities for a prolonged period and that recovery may occur if vigorous exercise is avoided.”
Another feather in the scale of acrylamide vs hyperglucose : vigorous exercise will decrease glucose faster than acrylamide.
3. This is a simple , but very clear experiment illustrating the links between acrylamide and diabetes .
The implications of this article are enormous . Is it true ? Has any other comparable experiments been done ?
The inference is that , taken together with the sub-chronic data about acrylamide , the chicken-and-egg situation between acrylamide and diabetes resolves to a “acrylamide first” picture .
In other words , the diabetic feedback condition is kicked off by prolonged sub-chronic acrylamide poisoning . While acrylamide does not accumulate in tissue or blood , the damage it does is repaired at a slower rate than ingestion . Diabetes seems to be an attempt of the body to get nutrients to nerve-extremities that have been cut off from supplies by axon-transport diminishment .
Instead of a disease , diabetes (at least at the start ) seems to be an attempt at a cure .
Curing it :
1.Cut all acrylamide ingestion . This means any food prepared at over 120 degrees Celsius or containing very small amounts ( micrograms ) of acrylamides (like canned olives , bottled prune juice , anything washed by lye)
2. Do not exercise vigorously until 8 days have passed since cutting all acrylamide ingestion .
3. Type II diabetes should taper off . (This needs to be proven.)
4. Take high concentrations of Evening Primrose Oil: the only clinically proven substance to reverse peripheral neuropathy . Obviously , it will only work well if intake of acrylamide is sharply reduced .
Attenuation of acrylamide-induced neurotoxicity in diabetic rats.Al Deeb S, Al Moutaery K, Arshaduddin M, Biary N, Tariq M.Neuroscience Research Group, Armed Forces Hospital, P.O. Box 7897 (W-912), Riyadh, Saudi Arabia.In recent years, an increasing number of cases of neuropathy have been reported as a result of accidental or occupational exposure to chemicals. Acrylamide (Acr), a widely used industrial chemical, is known to produce peripheral neuropathy that resembles diabetic neuropathy in many ways. However, the interaction between diabetes and Acr has not been studied. The present study was undertaken to examine the effect of streptozotocin (STZ)-induced diabetes on Acr-induced neurotoxicity in rats. Male Sprague-Dawley rats weighing 300 +/- 10 g were divided into four groups of 10 animals each. The rats in group 1 served as control, and received normal saline. The animals in group 2 were given Acr dissolved in physiological saline (50 mg/kg IP 3 days/week) for 2 weeks. The rats in group 3 and 4 were made diabetic by administering a single IP injection of STZ (50 mg/kg). The animals in group 3 served as diabetic control, whereas the rats in group 4 received Acr in the same dose regimen as in group 2, a week after induction of diabetes. Neurobehavioral responses including foot print length, hind limb function, landing foot splay, and the ability to stay on an inclined plane were assessed 48 h after the last dose of Acr followed by electrophysiological measurements. The animals were then sacrificed, and sciatic nerves were collected for biochemical analysis. The results of this study clearly showed a significant deterioration of neurobehavioral and electrophysiological responses in Acr-treated rats. Although no significant change in these parameters was observed in the diabetic (only) group, Acr-induced functional deficiency was significantly reduced in diabetic animals. However, the difference in electrophysiological response in Acr-treated diabetic and nondiabetic rats was not found to be statistically significant (p 0.05). The precise mechanism by which Acr induced neurobehavioral toxicity is reduced in diabetic animals warrants further investigations.PMID: 10758354 [PubMed - indexed for MEDLINE]
Happy eating
Andre
Friday, June 09, 2006
Training the Immune
Training the Immune System.
The immune system is capable of handling most diseases , but is primarily reactive . The initiative is with diseases causing rapid changes in the targeting markers . Two new powerful techniques , which works very well in synergy , have emerged :
Method :
1. Isolate some disease causing cells (ie cancerous cells , HIV , etc)
2.Slow the activity in the cells , thereby halting cell-wall changes , by using H2S concentrations graduated from (say) 75 ppm to 80 ppm.
3. Kill the cells using hypochlorous acid ( bleach ) .
Rationale :
1. The effect of H2S is well documented .
It slows the metabolism of the whole cell , including the cell-wall .
2. The effect of hypochlorous acid ( bleach ) :
Refer to
Cancer Immunology and Immunotherapy , Do1:10.007/s00262-006-0127—9
Or
New Scientist of 4 March 2006 p17 .
Cancer cells killed by hypochlorous acid (HOCl) ( bleach ) is five times more likely to be recognized as malign by dendritic cells than those killed by other means . This is an experimental fact .
The reason seems to be that one of the main methods by which the immune systems
kills deviant cells is by an injection of hypochlorous acid ( bleach ) . The fragments of hypochlorous acid mark the fragments of target cells as enemies to the immune system .
It is interesting to note that this seems to indicate a rapidly changing cell-wall structure for cancer cells , as there is a enemy-recognition , but not a very big one . This suggests the changeable cell-wall frozen at the moment of death does not encompass a large variety of the surface-configurations the cell can assume .
Hence we suggest a H2S concentration gradient up to stasis level to halt the various cell-wall permutations at various configurations at the moment of the hypochlorous acid kill . This should increase the immune system’s enemy recognition percentage .
The question remains why would the technique be more effective with H2S than without it ?
The answer is that these intractable diseases , by definition , has evolved anti-attack mechanisms . One of these would certainly involve rapid change in the surfaces of the cells . The cells in the treatment sample would quickly diverge from the body’s system . The body’s system would change slower because of signaling molecules (refer to quorum effect ) .
Thus , by immediately slowing the treatment sample by a graduated H2S concentration , killing it and immediately re-injecting , the immune system gains recognition of the enemy and hopefully some degree of advance on it .
The suspicion arises that a very simple molecule like HOCl is like other similarly simple molecules (nitrogen oxides , CO2 , etc that are used by living organisms as powerful signalling molecules .
HOCl kills any cell we know of . The only defense seems to be a thick shield . Is this wholly due to it’s reactive nature , or is there also a receptor site for it ? Immune cells kill by injecting it through a synapse-like structure . Thus , the targeting mechanism and the lethal payload share a linkage . This structure can learn through evolution .
Evolutionary speaking , the immune system will first try to kill by apoptosis as this is more economical . If this fails , then it will try to kill the cell by HOCl injection . If this fails and the system is still under stress , the chances are that it is a disease that is changing cell-walls quicker than the matching changes in the synapse-like immune cells mechanism .
The immune system will evolve two strategies :
First , try to decrease the change-speed in the attacking organism (first because this is older in evolutionary terms .)
Then , increase the learning speed of the immune system . Can you see where this is heading ?
Strategy 1 . Decrease in the change-speed in the attacking organism (whether internal like cancer or external like flu ) is handled by H2S type mechanisms . Hence the importance of sulfur ( see my previous notes ).
Strategy 2 . Increase the immune system’s learning speed.
Erk. This is a bit humbling .
On a basic level , Iodine seems to fill the requisite niche for a simple thing that has profound effects on the immune system , and thus on the nervous system .
The mechanism controlling the long-term , planet-wide distribution of sulfur and iodine is the algal organisms in the upper levels of the oceans . These are very temperature-dependant .
As the planetary temperature rises , the average concentration of sulfur and iodine falls because the algae retreat to the poles . Diseases increase . The immune systems first try the H2S route (because this is older ) , then try increasing the learning speed . We see this as intelligence .
Thus , we can see the pulse of intelligence in human affairs after the end of the last ice-age as a direct result of the increase in diseases caused by the decrease in sulfur and iodine concentrations .
An example: It is generally thought that the increased fishing off African waters caused the Africans to eat more bush-meat , thereby increasing their exposure to exotic diseases . But they have been eating the same for thousands of years . The critical lack is iodine
To sum up , human increased intelligence can be seen as an immune-system response to periods of warm inter-glacials . Since there is small evolutionary pressure to decrease intelligence , the effect ratcheted up . At present , humans can be seen as part of the planetary response to the relentless warming of the sun .
In other words , a planet like Earth which started off slightly too cool about 3 billion years ago , reached ideal life-temperature about 2 billion years ago and has gradually heated up as the sun became hotter (it is now 25% hotter than 3 billion years ago) .
The life-systems on the planet formed a complex feedback system which kept the system at livable temperatures . (Cf Daisyworld , Gaia and similar models) .
It is important to realize that the insolation from the sun fluctuated . The higher influx from sol left less leeway on the upper end of the boundary for living organisms on earth . A bit hotter , and living things did not as well with as a bit cooler .
So , as the sun became hotter , the earth’s thermostat evolved to be cooler (to leave room for fluctuations on the hot side). Please note that no conscious agency is necessary . Living learning mechanisms like discussed above evolved and became more intelligent with each heat-burp .
Till eventually , we get the present situation . Humans will have to cool the planet or become extinct . This can be seen to be (nearly) inevitable from the first planetary configuration . Another way of looking at it that humans are a part of the life systems on the planet ensuring its continuation .
Humans are a result of the heating of the planet , not the cause .
Intelligence is inevitable on any planet around a star on the main sequence .
Andre
The immune system is capable of handling most diseases , but is primarily reactive . The initiative is with diseases causing rapid changes in the targeting markers . Two new powerful techniques , which works very well in synergy , have emerged :
Method :
1. Isolate some disease causing cells (ie cancerous cells , HIV , etc)
2.Slow the activity in the cells , thereby halting cell-wall changes , by using H2S concentrations graduated from (say) 75 ppm to 80 ppm.
3. Kill the cells using hypochlorous acid ( bleach ) .
- Inject the lot back into the organism .
- Repeat quickly.
Rationale :
1. The effect of H2S is well documented .
It slows the metabolism of the whole cell , including the cell-wall .
2. The effect of hypochlorous acid ( bleach ) :
Refer to
Cancer Immunology and Immunotherapy , Do1:10.007/s00262-006-0127—9
Or
New Scientist of 4 March 2006 p17 .
Cancer cells killed by hypochlorous acid (HOCl) ( bleach ) is five times more likely to be recognized as malign by dendritic cells than those killed by other means . This is an experimental fact .
The reason seems to be that one of the main methods by which the immune systems
kills deviant cells is by an injection of hypochlorous acid ( bleach ) . The fragments of hypochlorous acid mark the fragments of target cells as enemies to the immune system .
It is interesting to note that this seems to indicate a rapidly changing cell-wall structure for cancer cells , as there is a enemy-recognition , but not a very big one . This suggests the changeable cell-wall frozen at the moment of death does not encompass a large variety of the surface-configurations the cell can assume .
Hence we suggest a H2S concentration gradient up to stasis level to halt the various cell-wall permutations at various configurations at the moment of the hypochlorous acid kill . This should increase the immune system’s enemy recognition percentage .
The question remains why would the technique be more effective with H2S than without it ?
The answer is that these intractable diseases , by definition , has evolved anti-attack mechanisms . One of these would certainly involve rapid change in the surfaces of the cells . The cells in the treatment sample would quickly diverge from the body’s system . The body’s system would change slower because of signaling molecules (refer to quorum effect ) .
Thus , by immediately slowing the treatment sample by a graduated H2S concentration , killing it and immediately re-injecting , the immune system gains recognition of the enemy and hopefully some degree of advance on it .
The suspicion arises that a very simple molecule like HOCl is like other similarly simple molecules (nitrogen oxides , CO2 , etc that are used by living organisms as powerful signalling molecules .
HOCl kills any cell we know of . The only defense seems to be a thick shield . Is this wholly due to it’s reactive nature , or is there also a receptor site for it ? Immune cells kill by injecting it through a synapse-like structure . Thus , the targeting mechanism and the lethal payload share a linkage . This structure can learn through evolution .
Evolutionary speaking , the immune system will first try to kill by apoptosis as this is more economical . If this fails , then it will try to kill the cell by HOCl injection . If this fails and the system is still under stress , the chances are that it is a disease that is changing cell-walls quicker than the matching changes in the synapse-like immune cells mechanism .
The immune system will evolve two strategies :
First , try to decrease the change-speed in the attacking organism (first because this is older in evolutionary terms .)
Then , increase the learning speed of the immune system . Can you see where this is heading ?
Strategy 1 . Decrease in the change-speed in the attacking organism (whether internal like cancer or external like flu ) is handled by H2S type mechanisms . Hence the importance of sulfur ( see my previous notes ).
Strategy 2 . Increase the immune system’s learning speed.
Erk. This is a bit humbling .
On a basic level , Iodine seems to fill the requisite niche for a simple thing that has profound effects on the immune system , and thus on the nervous system .
The mechanism controlling the long-term , planet-wide distribution of sulfur and iodine is the algal organisms in the upper levels of the oceans . These are very temperature-dependant .
As the planetary temperature rises , the average concentration of sulfur and iodine falls because the algae retreat to the poles . Diseases increase . The immune systems first try the H2S route (because this is older ) , then try increasing the learning speed . We see this as intelligence .
Thus , we can see the pulse of intelligence in human affairs after the end of the last ice-age as a direct result of the increase in diseases caused by the decrease in sulfur and iodine concentrations .
An example: It is generally thought that the increased fishing off African waters caused the Africans to eat more bush-meat , thereby increasing their exposure to exotic diseases . But they have been eating the same for thousands of years . The critical lack is iodine
To sum up , human increased intelligence can be seen as an immune-system response to periods of warm inter-glacials . Since there is small evolutionary pressure to decrease intelligence , the effect ratcheted up . At present , humans can be seen as part of the planetary response to the relentless warming of the sun .
In other words , a planet like Earth which started off slightly too cool about 3 billion years ago , reached ideal life-temperature about 2 billion years ago and has gradually heated up as the sun became hotter (it is now 25% hotter than 3 billion years ago) .
The life-systems on the planet formed a complex feedback system which kept the system at livable temperatures . (Cf Daisyworld , Gaia and similar models) .
It is important to realize that the insolation from the sun fluctuated . The higher influx from sol left less leeway on the upper end of the boundary for living organisms on earth . A bit hotter , and living things did not as well with as a bit cooler .
So , as the sun became hotter , the earth’s thermostat evolved to be cooler (to leave room for fluctuations on the hot side). Please note that no conscious agency is necessary . Living learning mechanisms like discussed above evolved and became more intelligent with each heat-burp .
Till eventually , we get the present situation . Humans will have to cool the planet or become extinct . This can be seen to be (nearly) inevitable from the first planetary configuration . Another way of looking at it that humans are a part of the life systems on the planet ensuring its continuation .
Humans are a result of the heating of the planet , not the cause .
Intelligence is inevitable on any planet around a star on the main sequence .
Andre
Primitives_0
Primitives _0
http://andreswhy.blogspot.com
Dated 7/06/2006
Quantity has a quality of its own (Stalin)
Background:
An example illustrates :
The visual system works well by having multiple small , very rapid recognition centers that recognise edges , corners , curves , etc . These are then assembled into further complex images further up the line to the brain .
A single neuron one or two layers away from this first primitive can handle surprisingly sophisticated pattern recognition ( eg bees trained to recognise human faces , only one neuron activating on fMRI scan on recognising a face)
The Advantages:
Note that the latest findings indicate that the only difference between animals and humans is the speed and capacity at which we perform tasks like planning , memory , tool usage , etc .
Also note that there is a fundamental correlation on neural-network level between speed and capacity . ( Hence the time-constraints in exams , IQ tests , sports ,ets)
Since we know that the minimum necessary sufficient number of dimensions in an Euclidean space is three , we can say that any visual system would work which has three layers . The more data is processed in each succeeding layer , the better , as long as there is a time-difference between viewpoints .
The Disadvantage
Definition :
A system lacking a primitive needed to recognise a new factor in the environment might not pick it up . Most primitives are learned in very early childhood and fixated by paring of neural connections on a hardware level . Eg Chinese “r” and “l” problems .
In other words , it is difficult for an adult to learn new languages , accents or to correct faulty visual systems .
Examples of Human Primitives:
Existing primitives:
1.Visual ( Retina-brain)
This ability would normally evolve into intelligent planning capability if there is sufficient number of neurons . Birds were first , but are constrained by a terrible evolutionary trap : in a low density atmosphere like Earth , their maximum weight ,and hence cranial capacity , is limited . They have a ceiling . If they go flightless , without hands they will lose the trajectory primitive , since the ability to compute trajectories will have no survival value . They optimise (like smart crows ) , but generalization is constrained by cranial size .
Start Speculation
The KT impact would have made no difference in Terran civilization , except that the civilized species would have descended from tree-dwelling dinosaurs . (See argument about insolation fibrillations and Gaia driving intelligence development. ) . Alien intelligent avians would possible if the atmospheric density is high enough to support birds with big brains . An estimate would be 6 to 8 times Terran densities at the moment . A planet like Venus would always have a denser atmosphere ( no large moon) . If there is life in a solar system , it would be seeded on all the planets by meteor impacts . Hence we can speculate that intelligent life on Venus evolved first from an avian base . Since the insolation fibrillations would have hit Venus first (because of its thicker atmosphere) , intelligence would have evolved there first in the solar system . Estimated time about 600 – 1000 million years before present . So where are they now ?
They are either extinct (most likely) , or the planet-bound ones are on Saturn . The clouds of Saturn would be very attractive to an avian species .
End Speculation
Apes coming out of the trees already had hands that could throw projectiles and had to have the trajectory primitive .
Hence , the evolution of upright stance ( to keep the hands free for throwing stones ) and stone using ( leading to neolithic technology ) came first and then led to further time-binding developments like planning , language and intelligence .
Notice that any human society , present and historical , spent an inordinate percentage of resources on trajectory games ( basically ball games) . It is pure Darwinnian statistics : good ballplayers have better time-binding primitives and are better at estimating future effects .
A good ball-player is not more successful because he is a team-player . He is a better team-player because he binds time better . Competition within co-operative boundaries .
Arrghh!
See Itarin for the nerd’s revenge .
2.Language : the primitives ( Broca’s area) are well established .
3.Fairness : Hardwired even into monkeys .
4.Math : count to 3 , rapidly and iteratively .
5.Threat avoidance : Hippocampus (Stress syndromes)
6.Balance (walking . ref vibrating soles.)
7.Creativity (not just LH/RH brain : it is a true primitive)
8.Music (inherent)
9.Risk/Reward : Profit . Making money (there has been heavy selection for this since the invention of agriculture ( ie surpluses)
10.Shapes (female hip , breast .Male buttocks , legs)
11. Pheromones
12. Immune system.
13. Religion
I’m sure there are more , but we know that these true primitives . Small , fast , multiple (mostly hardwired) data-handling nodes feeding into more sophisticated feedback systems.
2. Primitives we would like to have .
A wish list.
Note that we might have the sensors for the desired characteristic , but not the primitive . The primitive would only evolve if there was an evolutionary pressure for it .
The general principle is that , if a primitive has not evolved , it can be created by using some existing structure and building on that .
Andre
-------------------------------------
http://andreswhy.blogspot.com
Dated 7/06/2006
Quantity has a quality of its own (Stalin)
Background:
An example illustrates :
The visual system works well by having multiple small , very rapid recognition centers that recognise edges , corners , curves , etc . These are then assembled into further complex images further up the line to the brain .
A single neuron one or two layers away from this first primitive can handle surprisingly sophisticated pattern recognition ( eg bees trained to recognise human faces , only one neuron activating on fMRI scan on recognising a face)
The Advantages:
- Speed . This is all-important in a survival driven organism .
Note that the latest findings indicate that the only difference between animals and humans is the speed and capacity at which we perform tasks like planning , memory , tool usage , etc .
Also note that there is a fundamental correlation on neural-network level between speed and capacity . ( Hence the time-constraints in exams , IQ tests , sports ,ets)
- Reduction in complexity . You need fewer neurons to do the same task . Most of the number of input data are used in the first primitive layer , which is usually hardwired (ie retina) to be very fast . The subsequent neural-network layers need orders of magnitude fewer nodes . The assembly over time of different viewpoints in these primitive snapshots ( ie the differences) will pick up the elements missing in each snapshot due to poor resolution .
Since we know that the minimum necessary sufficient number of dimensions in an Euclidean space is three , we can say that any visual system would work which has three layers . The more data is processed in each succeeding layer , the better , as long as there is a time-difference between viewpoints .
The Disadvantage
Definition :
A system lacking a primitive needed to recognise a new factor in the environment might not pick it up . Most primitives are learned in very early childhood and fixated by paring of neural connections on a hardware level . Eg Chinese “r” and “l” problems .
In other words , it is difficult for an adult to learn new languages , accents or to correct faulty visual systems .
Examples of Human Primitives:
Existing primitives:
1.Visual ( Retina-brain)
- Pattern recognition (lines , edges curves,etc)
- Peripheral movement (snapshot differences )
- Linear Trajectory (integration of eye and body movement in snapshot differences. Very high speed required . ) This is the ur time-binding primitive . How the past and the projected future connect .
This ability would normally evolve into intelligent planning capability if there is sufficient number of neurons . Birds were first , but are constrained by a terrible evolutionary trap : in a low density atmosphere like Earth , their maximum weight ,and hence cranial capacity , is limited . They have a ceiling . If they go flightless , without hands they will lose the trajectory primitive , since the ability to compute trajectories will have no survival value . They optimise (like smart crows ) , but generalization is constrained by cranial size .
Start Speculation
The KT impact would have made no difference in Terran civilization , except that the civilized species would have descended from tree-dwelling dinosaurs . (See argument about insolation fibrillations and Gaia driving intelligence development. ) . Alien intelligent avians would possible if the atmospheric density is high enough to support birds with big brains . An estimate would be 6 to 8 times Terran densities at the moment . A planet like Venus would always have a denser atmosphere ( no large moon) . If there is life in a solar system , it would be seeded on all the planets by meteor impacts . Hence we can speculate that intelligent life on Venus evolved first from an avian base . Since the insolation fibrillations would have hit Venus first (because of its thicker atmosphere) , intelligence would have evolved there first in the solar system . Estimated time about 600 – 1000 million years before present . So where are they now ?
They are either extinct (most likely) , or the planet-bound ones are on Saturn . The clouds of Saturn would be very attractive to an avian species .
End Speculation
Apes coming out of the trees already had hands that could throw projectiles and had to have the trajectory primitive .
Hence , the evolution of upright stance ( to keep the hands free for throwing stones ) and stone using ( leading to neolithic technology ) came first and then led to further time-binding developments like planning , language and intelligence .
Notice that any human society , present and historical , spent an inordinate percentage of resources on trajectory games ( basically ball games) . It is pure Darwinnian statistics : good ballplayers have better time-binding primitives and are better at estimating future effects .
A good ball-player is not more successful because he is a team-player . He is a better team-player because he binds time better . Competition within co-operative boundaries .
Arrghh!
See Itarin for the nerd’s revenge .
2.Language : the primitives ( Broca’s area) are well established .
3.Fairness : Hardwired even into monkeys .
4.Math : count to 3 , rapidly and iteratively .
5.Threat avoidance : Hippocampus (Stress syndromes)
6.Balance (walking . ref vibrating soles.)
7.Creativity (not just LH/RH brain : it is a true primitive)
8.Music (inherent)
9.Risk/Reward : Profit . Making money (there has been heavy selection for this since the invention of agriculture ( ie surpluses)
10.Shapes (female hip , breast .Male buttocks , legs)
11. Pheromones
12. Immune system.
13. Religion
I’m sure there are more , but we know that these true primitives . Small , fast , multiple (mostly hardwired) data-handling nodes feeding into more sophisticated feedback systems.
2. Primitives we would like to have .
A wish list.
Note that we might have the sensors for the desired characteristic , but not the primitive . The primitive would only evolve if there was an evolutionary pressure for it .
- Spin
- Controlling the potentiating of hippocampus , immune system or any other primitive . A meta-primitive .
- Recognising and controlling quantum events .
- Recognising and controlling disequilibrium events
- Recognise and predict chaotic attractors.
- Sense and manipulate magnetic fields .
- Sense and manipulate nuclear fields .
- Sense and manipulate gravitational fields .
The general principle is that , if a primitive has not evolved , it can be created by using some existing structure and building on that .
Andre
-------------------------------------
Neuropathy
Diabetic Peripheral Neuropathy and Acrylamide
http://andreswhy.blogspot.com
Dated 11/06/2006
Background:
See links at the bottom .
Acrylamide is formed by the Maillard reaction , when the Amino Acid Asparigine reacts with reducing sugars like glucose and fructose at a temperature over 120 degrees Celsius . (ie when bread , potatoes , cookies , etc begin to brown ).
Asparigine + glucose/fructose + (temp>120 Celsius) = Acrylamide
Acrylamide is a potent neurotoxin . It interferes with the internal neuronal transport in the axon . The transport of nutrients from axon nucleus to the end point of the nerve and the return of breakdown products of long nerves ( like to fingers and toes ) are first affected . The ends of the axon start to die . ( Numbness in extremities . )
Sensations of restlessness , tingling , burning , etc associated with peripheral neuropathy are probably caused by the spurious signals caused by the accumulation of debris at the interference site in the charge balance of the axon wall .
( Think train derailment in the middle of the Karoo , with the smashed up carriages messing up the signalling system )
Since many non-diabetics have peripheral neuropathy , the two diseases do not seem to be directly linked . But a synergistic link is strongly suspected .
But if you are diabetic and already have had attacks of peripheral neuropathy , ingesting high concentrations of acrylamide will surely lead to an attack of peripheral neuropathy .
Note the short half-life of acrylamide means that the concentration of acrylamide is driven by diet alone .
Asparigine , glucose/fructose , (temp>120 Celsius) are all three necessary to produce Acrylamide . Hence foods low on the first two , or cooked below 120 Celsius are safe .
The EU study found that 90% of diet derived acrylamide comes from :
French Fries (slap chips) : 16% – 30%
Potato crisps : 6% - 46%
Coffee (its always roasted ) : 13% - 39%
Pastries and Sweet biscuits : 10% - 20%
Bread , breadrolls , pizza and toast (especially the crust) : 10% - 30%
In general , avoid anything that used a temperature of 120 Celsius or above in it’s preparation . This includes teas .The effective concentrations of acrylamide needed to trigger the reaction is very low , especially for diabetics already sensitized .
Anything low GI microwaved submerged in water , or cooked without burning or browning should be ok .
Durum pastas should be ok , but no grills or ovens . Bye-bye toasted cheese sandwiches .
Bread.
If you have to eat bread , cut off the crusts . Mothers used to do this for their children .
Any connection to attention Deficit Disorder ?
The irritability felt in the first stages of peripheral neuropathy ( ie wandering feet , can’t keep still ) and later on , irritable aggressiveness , sleeplessness and any activity to focus attention on anything except the painful feet ) sounds like the recipe for aggressive expansion .
Remember , that only the upper and middle classes ate bread . The bottom class (99 % of the population till about 1800 AD) ate porridge morning , noon and night. Milling kernels of wheat was ( and is ) expensive in real energy terms . (cf “Roman women will not grind wheat or cook “ after the Sabine episode , or lack of white bread in WW2) . Since it is a high energy food , it would be one of the great ironies of history that Empires and Inventions were caused by bread crusts . There is also a positive feedback element involved , namely that the type of wheat with the highest aspargine content will be the most widespread ( spread by the restless conquerors ) .
One wonders if the political instability inherent in the Middle East and North Africa are due to the high acrylamide content of their traditionally baked (from hot rock flat bread) foods . (In poorer regions like Europe , the plebs could not afford the energy cost .)
Hah! So much for meat . The weevilly baked biscuit of the middle ages was the driving force of the mariners to populate the earth with high-asparigine wheat .
No wonder things have gotten more unstable . For every diabetic , there are at least ten with an itchy , irritable nervosity .
Will humans use aspariginase ? This is an enzyme that destroys asparigine . Dosing food to a country with this will render them relatively docile in long run . Any volunteers ?
An interesting corollary is rice vs wheat . Rice is usually cooked at 100 Celsius . As the Chinese and Indian populations shift to high-arganine western wheat types , not only will their diabetes rates rise , but their aggression will rise at a much higher rate .
Interesting times for all .
Can one bake bread at less than 120 Celsius ?
See web references on Acrylamide:
1. PIM’s (1999) : The clinical picture .
http://www.inchem.org/documents/pims/chemical/pim652.htm
Some highlights:
Chronic exposure to Acrylamide:
Chronic acrylamide toxicity is characterized by local
dermatitis, excessive sweating, fatigue, weight loss and
features of progressive CNS disturbance (especially truncal ataxia) and peripheral neuropathy. The severity of symptoms and the rapidity of onset appears to relate to the duration of exposure to, and the daily dose of, acrylamide.
Recovery over a period of weeks to months following removal from exposure is the usual course.
Biological half-life by route of exposure
In blood, acrylamide has a half-life of approximately 2
hours. In tissues, total acrylamide (parent compound an
metabolites) exhibits biphasic elimination with an initial
half-life of approximately 5 hours and a terminal half life of 8 days (Edwards, 1975; Miller et al., 1982).
Acrylamide does not accumulate in the body. [Note: all data derived from animal studies].
2. On 25 April 2002 (cf New Scientist of 22 April 2006 p 8 ) , Sweden’s National Food Administration announced that acrylamide in significant concentrations was found in many common processed foods . This prompted a major clinical food study by the European Union : the results are given on the EU’s food site:
http://www.ciaa.be click on Documents , Positions , search on acrylamides from website .
----------------------------------------------------------------------------------------------------
http://andreswhy.blogspot.com
Dated 11/06/2006
Background:
See links at the bottom .
Acrylamide is formed by the Maillard reaction , when the Amino Acid Asparigine reacts with reducing sugars like glucose and fructose at a temperature over 120 degrees Celsius . (ie when bread , potatoes , cookies , etc begin to brown ).
Asparigine + glucose/fructose + (temp>120 Celsius) = Acrylamide
Acrylamide is a potent neurotoxin . It interferes with the internal neuronal transport in the axon . The transport of nutrients from axon nucleus to the end point of the nerve and the return of breakdown products of long nerves ( like to fingers and toes ) are first affected . The ends of the axon start to die . ( Numbness in extremities . )
Sensations of restlessness , tingling , burning , etc associated with peripheral neuropathy are probably caused by the spurious signals caused by the accumulation of debris at the interference site in the charge balance of the axon wall .
( Think train derailment in the middle of the Karoo , with the smashed up carriages messing up the signalling system )
Since many non-diabetics have peripheral neuropathy , the two diseases do not seem to be directly linked . But a synergistic link is strongly suspected .
But if you are diabetic and already have had attacks of peripheral neuropathy , ingesting high concentrations of acrylamide will surely lead to an attack of peripheral neuropathy .
Note the short half-life of acrylamide means that the concentration of acrylamide is driven by diet alone .
Asparigine , glucose/fructose , (temp>120 Celsius) are all three necessary to produce Acrylamide . Hence foods low on the first two , or cooked below 120 Celsius are safe .
The EU study found that 90% of diet derived acrylamide comes from :
French Fries (slap chips) : 16% – 30%
Potato crisps : 6% - 46%
Coffee (its always roasted ) : 13% - 39%
Pastries and Sweet biscuits : 10% - 20%
Bread , breadrolls , pizza and toast (especially the crust) : 10% - 30%
In general , avoid anything that used a temperature of 120 Celsius or above in it’s preparation . This includes teas .The effective concentrations of acrylamide needed to trigger the reaction is very low , especially for diabetics already sensitized .
Anything low GI microwaved submerged in water , or cooked without burning or browning should be ok .
Durum pastas should be ok , but no grills or ovens . Bye-bye toasted cheese sandwiches .
Bread.
If you have to eat bread , cut off the crusts . Mothers used to do this for their children .
Any connection to attention Deficit Disorder ?
The irritability felt in the first stages of peripheral neuropathy ( ie wandering feet , can’t keep still ) and later on , irritable aggressiveness , sleeplessness and any activity to focus attention on anything except the painful feet ) sounds like the recipe for aggressive expansion .
Remember , that only the upper and middle classes ate bread . The bottom class (99 % of the population till about 1800 AD) ate porridge morning , noon and night. Milling kernels of wheat was ( and is ) expensive in real energy terms . (cf “Roman women will not grind wheat or cook “ after the Sabine episode , or lack of white bread in WW2) . Since it is a high energy food , it would be one of the great ironies of history that Empires and Inventions were caused by bread crusts . There is also a positive feedback element involved , namely that the type of wheat with the highest aspargine content will be the most widespread ( spread by the restless conquerors ) .
One wonders if the political instability inherent in the Middle East and North Africa are due to the high acrylamide content of their traditionally baked (from hot rock flat bread) foods . (In poorer regions like Europe , the plebs could not afford the energy cost .)
Hah! So much for meat . The weevilly baked biscuit of the middle ages was the driving force of the mariners to populate the earth with high-asparigine wheat .
No wonder things have gotten more unstable . For every diabetic , there are at least ten with an itchy , irritable nervosity .
Will humans use aspariginase ? This is an enzyme that destroys asparigine . Dosing food to a country with this will render them relatively docile in long run . Any volunteers ?
An interesting corollary is rice vs wheat . Rice is usually cooked at 100 Celsius . As the Chinese and Indian populations shift to high-arganine western wheat types , not only will their diabetes rates rise , but their aggression will rise at a much higher rate .
Interesting times for all .
Can one bake bread at less than 120 Celsius ?
See web references on Acrylamide:
1. PIM’s (1999) : The clinical picture .
http://www.inchem.org/documents/pims/chemical/pim652.htm
Some highlights:
Chronic exposure to Acrylamide:
Chronic acrylamide toxicity is characterized by local
dermatitis, excessive sweating, fatigue, weight loss and
features of progressive CNS disturbance (especially truncal ataxia) and peripheral neuropathy. The severity of symptoms and the rapidity of onset appears to relate to the duration of exposure to, and the daily dose of, acrylamide.
Recovery over a period of weeks to months following removal from exposure is the usual course.
Biological half-life by route of exposure
In blood, acrylamide has a half-life of approximately 2
hours. In tissues, total acrylamide (parent compound an
metabolites) exhibits biphasic elimination with an initial
half-life of approximately 5 hours and a terminal half life of 8 days (Edwards, 1975; Miller et al., 1982).
Acrylamide does not accumulate in the body. [Note: all data derived from animal studies].
2. On 25 April 2002 (cf New Scientist of 22 April 2006 p 8 ) , Sweden’s National Food Administration announced that acrylamide in significant concentrations was found in many common processed foods . This prompted a major clinical food study by the European Union : the results are given on the EU’s food site:
http://www.ciaa.be click on Documents , Positions , search on acrylamides from website .
----------------------------------------------------------------------------------------------------