Alan Watts, Solid Emptiness.

wine good for you?

Is a glass or two of wine a day good for you?  You would think this would be an easy question to answer, but it's not, and that's because of this:
How many glasses of wine are in a bottle?
If you answered 4-5, continue reading.  Because guess what?  Apparently the answer is eight. No, I'm not kidding. Yes, they are serious.  Unplug your monitor and ram it into your skull as hard as you can.

"Doctors don't know.  They pretend to know.  Because they have a rectal thermometer in their pocket.  As if it were an appeal to a higher authority."-- Lewis Black 

It comes down to this: medicine doesn't have all the answers, but in presenting their recommendations it sounds like they do.  And we get confused.
"Two drinks a day."  What's a drink?  Are the health benefits/risks of whisky and wine identical?  Then why lump them together?  And if the answer is, "well, we don't know enough yet" then why are you making recommendations with the authority of medical certainty?
The reason wine's benefits/risks seem confusing is that no one emphasizes the size of a "drink."
A "drink" is often defined as 10g alcohol-- that's 1/8 of a bottle of wine. 
Many reference guides, in an attempt to make things simple to understand (if you're drunk, maybe) use 10g/drink as a standard. There are 750ml in a bottle of wine. If the bottle is 13% alcohol by volume, then there is 98ml alcohol per bottle. Alcohol's specific gravity is .79, so there are 77g alcohol in a bottle.   That means that there are 7-8 "drinks" in a bottle of wine, which, if I may editorialize, is so preposterous as to hardly merit comment.
Similarly, for 5% beer, there is 0.05 x355ml x 0.79= so 14g per 12 oz can.  Is a beer a drink and a half?
Alcohol content varies greatly among wines and beers:
Also, each wine has a different alcohol content-- 12.5% is the typical French ideal, and most wines are built (i.e. alcohol osmotically removed) to stay under 14% because the tariff increases above that.   There is a leeway of 1.5% in the listing, so 12.5% could be 11% or 14%.  That's a 2 "drink"/bottle difference.
In the past few years, and especially with California wines, Syrahs, Zinfandels, places with hot climates, the trend has been towards using higher Brix (sugar content) grapes.  (Riper means more sugar, which means more alcohol.)  About 55% of the sugar ferments to alcohol, and the common 25 Brix grapes convert to a 13.75% wine.  Plus you lose some water in the wine making process, so it may be even higher than that (15%).

To complicate things further, each policy group advocates different safe drinking levels that are nearly incomprehensible to the layman, unless you convert them to some common measure (here, I convert to grams):  The U.S. government says no more than 2 drinks per day-- but that's 14g each.  France says no more than 5  per day-- but it's 12g each.  Britain says 3-4 "units"-- at 8g each!  Do the British know this?  A British study (in Scots) found that people generally pour out two, not one, unit per drink.  It's no wonder people are confused.
A better conversion is this: there is 77g alcohol in a 13% bottle of wine.  That's equivalent to  almost a six pack.  Go.
Blood Alcohol Content: as accurate as a New York Times poll, but you can still go to jail.
Converting to grams as a reference for drinking is useful because it allows you to predict your BAC.  Here is how everyone tells you to calculate it:  If you drink 40g alcohol and weigh 70kg, your BAC will be .05% (40g/70000g).  Or, if you weigh 70kg, every 14g beer will raise your BAC by .02%  Or, every 1/4 bottle of wine raises the level .035%.  Isn't math fun?  I have seen countless "reference tables" using this method.
But the units of BAC are g alcohol/100ml water.  You're not all warer, are you?  You're about... 60% water?  So that 40g alcohol in really in 70kg x .6= 42kg water.  40g alcohol/42000ml water= .09%.  Congrats.  You're drunk.  Sort of.
In practice, those reference tables telling you your estimated BAC already incorporate the Widmark constant-- the percentage body water. It can range from 40-85% water.  The more water you have, the lower will be your BAC.  Women have less water, so their conversion runs lower (40-50%).  Muscle= more water; fat=less water. The problem, obviously, is while BAC calculations use a standard-- for example, my .6, above-- individuals can vary greatly.  Hence, lawyers.
But wait: Breathalyzers. It's measuring the alcohol content of your breath, not blood.  What's the ratio of alcohol in breath to blood?  2400:1?  2100:1?  Generally, breathayzers are calibrated to underread your alcohol level, by about 10%.  So even though most humans run 2400:1, it is calibrated at 2100:1.  But don't try to argue "individual variability" of a breathalyzer in court: 2100:1 is part of the statute, and thus your reading is your sentence.   But remember, liquid to gas transitions are described by Henry's coefficient: heating a substance (e.g. alcohol) puts more in the air (breath); cooling the air (breath) makes the substance stay in liquid (blood).  So before you blow into the machine, hyperventilate and roll in the snow.
The point here is that you-- and guidelines-- cannot predict your BAC based on how many "drinks" you had, because there are so many confounding variables.
Note that BAC doesn't tell you how drunk you are-- tolerance might mean you're an effective Lisp programmer at .1%, or you're beer goggling at .02%. At a given weight, higher percentage body fat= more drunk. Also, food delays absorption. Finally, some people metabolize alcohol faster than others; the old rule "a drink an hour" is based on the assumption that you metabolize 10g alcohol per hour (or your BAC falls by .01%/hr)-- but in you it may be 20g/hr (e.g. a daily drinker), or 5g/hr (e.g. young woman rarely drinks, on Tylenol) etc.

But legal driving limit is usually .08%.  And 50% of the time, .4% is death, so there's that.
Health Benefits of Wine?  Or No? 
So since the term "drink" is uselessly vague, in reviewing the literature on wine and beer's effects, I'll do my best to convert to grams of alcohol.  Just remember that a bottle of wine is 77g, and 12oz 5% beer is 14g.
Cholesterol, triglycerides, coronary artery disease: about half a bottle of wine, but at least 20g/d, raises HDL,;decreases TG, CRP, fibrinogen, and decreases risk of CAD.
Generally, moderate alcohol consumption (say, 30-40g/d) is associated with decreases in mortality.  This is hypothesized to be related to a) its HDL raising effect; b) its reduction of pro-inflammatory proteins CRP and fibrinogen (i.e. it's anti-inflammatory.)
One of the studies, in Nature,  that popularized "moderate consumption" was this: 40g/d (from beer) for men, 30g/d for women, reduced inflammatory markers C-reactive peptide (35%) and fibrinogen (12%),  increased HDL (10%), with no change in TG or liver enzymes.  after 3 weeks of drinking.   The study called this "four glasses" but a better way of understanding it is three beer cans or  half a bottle of wine.  Also: BAC 1 hour after drinks was 10mmol/l.  Yes, mmol.  Sigh.  46g/mol: BAL .046%
A prospective study confirmed the "well-known" relationship between alcohol consumption and HDL, which rose from 40 to 50 with >30g/d alcohol.
A German study of 7000+ people found HDL rose, and fibrinogen decreased,  for women who drank 10-20g/d and men >30g/d.
A Danish study found an interesting relationship: women who drank at least once per week had lower risk of CAD than abstainers; but drinking more often did not promote the effect.  But for men, daily drinking (more than less frequent drinking) was associated with the lowest risk.

Oxidative Stress: doesn't ethanol cause lipid peroxidation (free radicals?) Answer:  you're not drinking ethanol, you're drinking wine--which probably increases antioxidant capacity. 
This is how you get plaques: free radicals in your diet (e.g. cooked fat) promote LDL oxidation, which goes on to promote arterial plaque formation.  Free radical scavengers, such as Vitamin E, would lessen this effect-- but are consequently reduced.  Importantly, the LDL from a meal is more susceptible to oxidation than normally circulating (fasting) LDL.
Alcohol promotes oxidation in test tubes.  So why wouldn't it do so in people?  For example, a careful study controlled for many confounding variables that are associated with high or low alcohol intake-- such as smoking, vitamins, exercise, etc-- and found that the more alcohol consumed, the higher the oxidized LDL, with no change in HDL.  Where did the protective effect go?  One possibility jumps to mind: median consumption was 6g/d; and the above studies found the relationship with the higher "doses."  And you need to be a regular drinker: 96 hours after a single dose of wine there was no effect on LDL. Surely I've made this up?  No: 300ml red wine (better than 300ml white wine) inhibited oxidation (e.g. LDL oxidation).  The likely explanation is that even though alcohol can cause oxidative stress, wine-- and it's constituents (polyphenols, resveratrol, etc) may overwhelm this effect.  But you have to drink enough (>300ml) so that it overwhelms alcohol's effects (but not so much your wife leaves you.)
Additionally, wine's beneficial effects in preventing oxidative stress may be enhanced when you have more oxidative stress to begin with.  Take the easy case of eating a fatty meal.  The LDLs that result from this meal are  more likely to be oxidized than the normal  fasting LDLs  in circulation.  Drinking 400ml of wine with a meal made these post-meal LDLs more resistant to oxidation than even the existing LDL, and maintained the Vitamin E levels.  And in case you're a rat, in rats who were force fed a high cholesterol diet, wine reduced the cholesterol levels and improved antioxidant parameters. 
Not just meal related oxidative stress: 1/3 bottle of red wine a day for two months in people who just had angioplasty substantially increased antioxidant reactivity and decreased oxidative damage.  There is a logic to this: the lower your CRP, the better is your natural antioxidant capacity, and wine lowers CRP proportionally more if it is already high.  A glass of wine (or one espresso- how do you like that!)  was equivalent to an orange or 200g spinach in antioxidant capacity.

Homocysteine (which causes coronary plaques)?   Maybe it goes up a little, but that might not matter, especially if you're drinking wine.
42 men got to drink half a bottle of WHITE wine a day for a month: lower oxidation products (and coincident increase in free radical scavengers and HDL), but also increased homocysteine. 
A prospective study found that after 6 weeks of 30g/day of wine/beer/spirits, homocysteine levels were higher than in controls.  Folate levels were also lower (except in beer-- because beer has about 30ug folate/beer and0.1ug vitamin B6/beer.)  Folate and B12 are cofactors in the conversion (methylation) of homocysteine which is then broken down (sulphyrated) with vitamin B6 as a cofactor; so low folate/B12= high homocysteine.  Similarly, in chronic alcoholics homocysteine was much higher-- but less so with beer.
And again, but with 40g/d drinking wine and spirits for three weeks, homocysteine went up 9%.  Beer had no effect.  But B6 went up with all drinks (more with beer).  Not only does B6 facilitate homocysteine degradation, it is also an independent inverse risk factor for cardiovascular disease.
But perhaps amounts are relevant: in another prospective study, 1/2 bottle/d of red wine for two weeks had no effect on homocysteine, while doing the expected increase of HDL and antioxidant capacity.
A study using pig coronary arteries found that while homcysteine impaired endothelial cell relaxation, red wine negated this adverse effect. 
It appears that homocysteine goes up, but that doesn't translate to any increased cardiovascular risk because of some beneficial effects of the wine, which may include B6, antioxidants, increased HDL and increased antioxidant capacity.
Blood Pressure?  Answer: No serious effect below a bottle of wine a day. 
German study (above) finds <80g/d associated with <2 mmHg increase; >80g/d associated with  4-6mm Hg increases.  American Idol makes mine go up more.

Much of the negative data on blood pressure is perplexingly inaccurate. By "perpelxingly" I mean that the errors could not have simply been oversights, could they?  People are lumped together, as are quantities and types of alcohol, giving misleading results.  For example, in an article entitled, "Alcohol is Bad For Blood Pressure"-- seriously, that's the title of the scientific article-- the authors state:

Since then, large-scale prospective studies from Japan (6) and the US(7) have indicated that the risk of hypertension increases twofold with alcohol intake of 30–50 g/day or more. 

Hmm.  "Increases twofold."  I'm not sure what article they read, but reference 7 pretty clearly says the opposite:

Our principal finding was the association between the consumption of low to moderate amounts of ethanol (up to 3 drinks per day) and either the incidence of hypertension or increase in blood pressure levels in blacks. In white men, there was no evidence of an increase in systolic or diastolic blood pressure over time at this level of consumption. Similarly, for most beverages, a low to moderate intake of alcohol was not associated with a higher incidence of hypertension in white men and with an increased incidence in black men.

And later:

the observation that low amounts of alcohol intake may not increase blood pressure in most race-gender strata could lead to a more tolerant view of the consumption of alcohol in small amounts...

Black men who drank heavily had double the incidence of hypertension (defined as a jump to > 140/90): 15% vs. to 30% in drinkers.  But I should add that the risk was relevant only in black men who drank beer or spirits; only 8 out of 250+ drank any wine at all.
Thus, blood pressure is minimally affected by wine, and even beer or spirits, if other variables are controlled.  There is a negative effect of beer and spirits in blacks that needs to be explored, as does the effect of wine in blacks.

Pancreatitic disease: How many drinks before you're in trouble? Answer: >30% of your daily calories from alcohol if you poor nutrition; or  >1 bottle wine/day for 25 years, especially if you eat like a pig.   Smoking=death.  (But you knew that.)
You'd be amazed at how hard this simple question was to answer.
As an aside, almost every study done in 2005-2007 on alcohol and pancreatic disease was done in Japan or China.  I'm sure there's a reason for this, but for the life of me I can't tell you what it is.  And if someone is able to explain to me how the Japanese and Chinese physiologies are generalizable to everyone, I'd like to hear it; but that's what happens.
The main problem with the studies is that risks of pancreatitis are associated with an arbitrary cut off that does not reflect the actual toxicity of alcohol.  For example, a study found that >2 drinks/d, compared to <2 drinks/d, was significantly associated with pancreatic necrosis.  So we're all going to die? The problem is that this association was either/or, not calibrated to amount.  For example, what if those who had the necrosis all drank more than 10drinks/d?  It would still be true that the risk was higher at >2 drinks/d.  So why 2/d as the cutoff? "The cutoff of two drinks per day was selected based on animal studies which have shown that the equivalent consumption of two drinks per day in rats results in measurable change in pancreatic histology and physiology(13)."  So, of course, I looked up (13): in rats who received 12%, and worse with 36% of their calories from alcohol increased pancreatic protein hypersecretion, starting the road to pancreatitis.  If you eat 2000 calories a day, then this would be equivalent to a little more than 1 bottle of wine/d.
A Japanese study found that the traditional rates of pancreatitis among alcoholics-- 2-5%-- may be low: they find that  9-17% of people who drank >150g alcohol/d developed alcoholic pancreatitis.  The alcoholic pancreatitis patients began drinking at a younger age (18), drank for 20 years) and drank 180g/d alcohol.  Additionally, they cite other studies where meat and lipid may be co-factors.
An interesting study found the risk of acute pancreatitis may be increased in the first day of withdrawal of drinking; these drinkers had drank an average of 700g/week (400-900g), and 3600/two months.  Alcohol suppresses inflammation, so this may be a rebound inflammatory response.
A Chinese study found that smoking, high meat and heavy drinking was associated with pancreatic cancer.  Heavy drinking was ">20 cup-years;" basically, 11g/d for 20 years, or 22 g/d for 10 years, etc.  The article did not address the hihger rates od ALDH2*2 allele of aldehyde dehydrogenase in the Chinese, which slows the metabolism of aldehyde (and allows it to build up-- see below.)
Another Japanese study (come on) found risk increased 10 fold for >100g/d, and >30 years of drinking.
Alcohol alone is not a risk factor for pancreatic ductal adenocarcimona, which is most closely associated with smoking.  Alcohol may indice pancreatitis and diabetes, which are themselves risk factors.  Also, acetaldehyde, an intermediary metabolite of alcohol which is ordinarily quickly metabolized to acetic acid, is procarcinogenic;  heavy drinkers with cancer, vs. alcoholics without cancer, had higher salivary aldehyde levels due to fast metabolism of alcohol to aldehyde. (I SPECULATE that binge drinking, and frequent exposure to acetaldehyde (read: hangovers) is more dangerous than low but daily drinking.)
Finally, you should know that many studies describing the risks of alcohol are not able to control well for smoking, which is a major risk factor.  Consider that 60% of chronic pancreatitis cases are smokers; but 80% of alcoholic chronic pancreatitis cases are smokers. And high BMI is a risk.
Diet and alcohol: in animal models of alcohol induced pancreatic disease, & calories due to alcohol is the measure.  For example, one mouse model uses 24%, and the mice had BAL 100mM (.46%). Most animal modesl use about 30%.  One study disputed the high protein/high fat risk of pancreatitis by finding that humans with pancreatic or liver disease took 50% of their calories as alcohol, and the worst cases had the highest percentage intake. A study in Mexico found high overall caloric intake (4110 vs. 2250 in healthy controls)  was the risk factor, but dividing the average daily alcohol (124g=868 cal) by calories (4110) gives you 21% calories from alcohol.
The type of alcohol here is not described. Was it red wine?  Vodka?  Beer?  You decide.

So there are two prongs: high caloric intake, especially from fats and protein, and consequent high BMI, along with alcohol (>100g/d, conservatively;) or poor nutritional intake with higher proportion of alcohol calories (>30%).  With both, smoking is a profound risk factor, especially for cancer.
Stop smoking.

Resveratrol:
Resveratrol (a type of estrogen (DES)) is a polyphenol contained in wine (and fruits, grapes, etc.,)  that is itself anti-inflammatory and antithrombogenic (it's a COX1-- COX2?-- inhibitor), as well as possibly being neuroprotective. It probably is an anti-flu drug. It can possibly prolong life span through SIRT1 (which is how calorie restriction prolongs life.)    Resveratrol is one possible explanation for why the French can eat fried butter sandwiches with a bottle of wine and still tell their grandkids about it.
There is no accepted dose.  A bottle of red contains about 1mg, unless you're drinking muscadine wine (Florida grapes, some ports, etc.) It appears to have no toxicities.
I bring it up here only to tell you that as much as I think resveratrol is super and all, it oxidizes very quickly after the bottle is opened.  So drink fast.
Calories:
There are 7 calories/gram alcohol.  So each bottle of wine has about 550 calories.  Each light beer is 110 calories.  There are about 50 calories in a shot of whisky.
Summary And Conclusions: 
Disclaimer: I'm not recommending anything to anyone, I'm not your doctor, results may vary, substantial penalty for early withdrawal (HA!).  Don't drink if you have GI disease.  Or if you drive.  Or if you're on medications.  Or if you're an idiot.  Especially if you're an idiot.
But it appears to me that 30-40g (1/3- 1/2 bottle) of wine alcohol a day is fine.  Enjoy it.  (Unfortunately, I'm a whisky guy.)  It seems to work best if you drink it with food.  Everyone else should just mellow the hell out.  This unprioritized rigidity, this obsession, with "health" and "prevention" is idiotic and counterproductive.  Today I cooked my family bacon and eggs.  BACON.  Take that, AMA's beliefs.
Some caveats:  most of the association studies, above, do their best to control for confounding factors, but sometimes this is impossible.  As a basic generalization, the person who drinks 1/2 bottle wine with dinner is likely to have a very different life than one who drinks 4 beers/day after work, notwithstanding the obvious confounding variable of alcohol with/without food.  So it may be impossible to say that wine, itself, is what is beneficial.
Despite this-- and why this is relevant to a psychiatry blog-- the error is to assume that one is "the type of person who drinks wine, and so would have lower risks" vs. "the type of person who drinks beers, and so would have higher risks."   It may be more accurate to consider that if one chooses to become the person who drinks wine with dinner instead of beer after work, a variety of other factors may also change.  As a simple example: beer at a bar is conducive to smoking, wine at home isn't.  Beer after work every day may be sabotaging your family life; a choice to switch to wine at dinner may improve things at home.  &c., &c.
This is important.  It is the thesis of this blog: nothing matters more than your will.  Even if wine and beer are themselves of no consequence to one's health, the lifestyle that follows with the conscious choice to drink either one is of consequence.  Every choice you make influences your identity, and not the other way around; the sooner you accept this, the sooner you can become the person you want to be. You get to pick who you are.  Go pick. 

(State laws prevent me from receiving donations of wine (or whisky.)  My drink is Balvenie 15 year.  It's about $65. Just saying.)

Tomiki

Nee-Me-Poo

Tell General Howard I know his heart. What he told me before I have in my heart. I am tired of fighting. Our chiefs are killed. Looking Glass is dead. Tu-hul-hul-sote is dead. The old men are all dead. It is the young men who say yes or no. He who led the young men [Ollokot] is dead. It is cold and we have no blankets. The little children are freezing to death. My people, some of them, have run away to the hills, and have no blankets, no food; no one knows where they are – perhaps freezing to death. I want to have time to look for my children and see how many of them I can find. Maybe I shall find them among the dead. Hear me, my chiefs. I am tired; my heart is sick and sad. From where the sun now stands I will fight no more forever.

Hin-mah-too-yah-lat-kekt

The first documented contact between the Nee-Me-Poo and white men occurred in 1805-6, when the Meriwether Lewis and William Clark army expedition to the Pacific passed through their lands, received assistance from them, and collected initial information about them. Subsequent exploring parties, principally those of the establishing fur companies, provided additional data. Early French-Canadian observers called the Nee-Me-Poo "Nez Perces" (pronounced in French "Nay-pair-SAY," but later anglicized to today's "Nez Purse"), in actuality a term prescribed for numerous groups who pierced their noses with dentalium shells. And although the Nee-Me-Poo apparently never practiced this custom extensively, they nonetheless retained the name. A brave, intelligent, and spiritual people, they had occupied their home territory for millennia, with archeological evidence reaching back for as many as thirteen thousand years. In their traditions, the people believe that they have been here since the time the world was first populated. They lived in several modes of housing, notably rush mat lodges, pine-board structures, and large semi-subterranean bark-covered dwellings, all capable of accommodating several families. Linguistically, the Nee-Me-Poo were of the Penutian language group and spoke a Sahaptian dialect, as did neighboring tribes of the Columbia Plateau. Like the mostly sedentary groups to the west, the Nee-Me-Poo traditionally subsisted on salmon, but they also hunted game in the forests and prairies and consumed local berries, roots, and tubers, especially relishing those of the camas and kouse plants.

Hin-mah-too-yah-lat-kekt, popularly known as Chief Joseph, or Young Joseph (March 3, 1840 – September 21, 1904) was the leader of the Wal-lam-wat-kain (Wallowa) band of Nez Perce during General Oliver O. Howard's attempt to forcibly remove his band and the other "non-treaty" Nez Perce to a reservation in Idaho. For his principled resistance to the removal, he became renowned as a humanitarian and peacemaker.

The non-treaty Nez Perce suffered many injustices at the hands of settlers and prospectors, but out of fear of reprisal from the militarily superior Americans, Joseph never allowed any violence against them, instead making many concessions to them in hopes of securing peace.
In 1873, Joseph negotiated with the federal government to ensure his people could stay on their land in the Wallowa Valley. But in 1877, the government reversed its policy, and Army General Oliver Howard threatened to attack if the Wallowa band did not relocate to the Idaho Reservation with the other Nez Perce. Joseph reluctantly agreed. General Howard held a council to try to convince Joseph and his people to relocate. Joseph finished his address to the General, which focused on human equality, by expressing his "[disbelief that] the Great Spirit Chief gave one kind of men the right to tell another kind of men what they must do." Howard reacted angrily, interpreting the statement as a challenge to his authority. When Toohoolhoolzote protested, he was jailed for five days.

Returning home, Joseph called a council among his people. At the council, he spoke on behalf of peace, preferring to abandon his father's grave over war. Toohoolhoolzote, insulted by his incarceration, advocated war. The Wallowa band began making preparations for the long journey, meeting first with other bands at Rocky Canyon. At this council too, many leaders urged war, while Joseph argued in favor of peace. While the council was underway, a young man whose father had been killed rode up and announced that he and several other young men had already killed four white settlers. Still hoping to avoid further bloodshed, Joseph and other non-treaty Nez Perce leaders began moving people away from Idaho.

With 2,000 U.S. soldiers in pursuit, over 800 Nez Perce went north in an attempt to reach Canada. For over three months, the Nez Perce outmaneuvered and battled their pursuers traveling 1,170 miles (1,900 km) across Oregon, Washington, Idaho, Wyoming, and Montana. General Howard was impressed with the skill with which the Nez Perce fought, using advance and rear guards, skirmish lines, and field fortifications. Finally, after a devastating five-day battle during freezing weather conditions with no food or blankets, with the major war leaders dead, Joseph formally surrendered to General Nelson Appleton Miles on October 5, 1877 in the Bear Paw Mountains of the Montana Territory, less than 40 miles (60 km) south of Canada in a place close to the present-day Chinook in Blaine County. The battle is remembered in popular history by the words attributed to Joseph at the formal surrender:

Tell General Howard I know his heart. What he told me before, I have it in my heart. I am tired of fighting. Our chiefs are killed; Looking Glass is dead, Too-hul-hul-sote is dead. The old men are all dead. It is the young men who say yes or no. He who led on the young men is dead. It is cold, and we have no blankets; the little children are freezing to death. My people, some of them, have run away to the hills, and have no blankets, no food. No one knows where they are—perhaps freezing to death. I want to have time to look for my children, and see how many of them I can find. Maybe I shall find them among the dead. Hear me, my chiefs! I am tired; my heart is sick and sad. From where the sun now stands, I will fight no more forever.^[8]

The popular legend deflated, however, when the original pencil draft of the report was revealed to show the handwriting of the later poet and lawyer Lieutenant Charles Erskine Scott Wood, who claimed to have taken down the great chief's words on the spot. In the margin it read, "Here insert Joseph's reply to the demand for surrender"^[9][10] Although Joseph was not technically a war chief and probably did not command the retreat, many of the chiefs who did had died.

Colonel Miles left Fort Keogh on September 18 with a force of 520 soldiers, civilian employees, and scouts, including about 30 Indian scouts, mostly Cheyenne but with a few Lakota (Teton Sioux).^[14] Some of the Indian scouts had fought against Custer in the Battle of the Little Big Horn only 15 months earlier, but had subsequently surrendered to Miles.^[15]

Miles was anxious to get involved in the pursuit of the Nez Perce and marched expeditiously north-west. He hoped to find the Nez Perce south of the Missouri River. His first destination was the mouth of the Musselshell River and from there he planned to move up the south bank of the Missouri. At the Missouri, Miles was joined by scout Luther “Yellowstone” Kelly. On September 25, Miles received a dispatch informing him of the Cow Creek fight and that the Nez Perce had crossed the Missouri going north. He changed his plans, crossed the Missouri, and headed toward the northern side of the Bear Paw Mountains passing the east side of the Little Rocky Mountains. Miles made every effort to keep his presence unknown to the Nez Perce whom be believed were only a few miles to his west. ^[16]

On September 29, several inches of snow fell. That day, Miles’ Cheyenne scouts found the trail of the Nez Perce and a few soldiers and civilian scouts had a skirmish with Nez Perce warriors. The next morning the Cheyenne found the Nez Perce encampment on Snake Creek north of the Bear Paw mountains. Miles soldiers advanced toward it.^[17]

That same day, scouts reported to the Nez Perce leaders the presence of a large number of people to their east. Most of their leaders wished to continue quickly on toward Canada, but Looking Glass prevailed. The people seen, he said, must be other Indians. Assiniboine and Gros Ventre were known to be hunting in the area. Consequently, the Nez Perce went into camp on Snake Creek only 42 miles (70km) from Canada and slowly the next morning, September 30, prepared to continue their journey.^[18]

Miles hurried his attack on the Nez Perce camp for fear that the Indians would escape. At 9:15 a.m, while still about six miles from the camp, he deployed his cavalry at a trot, organized as follows: the 30 Cheyenne and Lakota scouts led the way, followed by the 2nd cavalry battalion consisting of about 160 soldiers. The 2nd cavalry was ordered to charge into into the Nez Perce camp. The 7th cavalry battalion of 110 soldiers followed the 2nd as support and to follow the 2nd on the charge into the camp. The 5th Infantry (mounted on horses) of about 145 soldiers followed as a reserve with a Hotchkiss gun and the pack train. Miles rode with the 7th cavalry.^[19]

Miles was following a tried and true tactic of the U.S. army in fighting Plains Indians: attack a village suddenly and “shock and demoralize all the camp occupants – men, women, and children, both young and old – before they could respond effectively to counter the blow.” ^[20] However, the Nez Perce were warned by scouts of the approach of the soldiers a few minutes in advance. They were scattered, some gathering up the horse herd, west of the encampment, others packing to leave. Some men quickly gathered to defend the encampment while 50 to 60 warriors and many women and children rushed out of the village to attempt an escape to the north and Canada.^[21]

Miles’ plan fell apart quickly. Rather than attacking the camp, the Cheyenne scouts veered to the left toward the horse herd and the 2nd Cavalry, commanded by Captain George L. Tyler, followed them. The Cheyenne and Tyler captured most of the horse herd of the Nez Perce and cut off from the village about seventy men, including Chief Joseph, plus women and children. Joseph told his 14 year old daughter to catch a horse and join the others in a flight toward Canada. Joseph, unarmed, then mounted a horse and rode through a ring of soldiers back into the camp, several bullets cutting his clothing and wounding his horse.^[22]

Tyler’s detour to the horse herd eliminated him from the van of the advancing soldiers and the main battle. He detached one company to chase the Nez Perce heading toward Canada. The company pursued the Nez Perce about five miles and then retreated as the Nez Perce organized a counter-attack. Once the women and children were safely out of reach of the soldiers some of the Nez Perce warriors came back to join their main force.

While the Cheyenne, Tyler, and the 2nd Cavalry were chasing horses, the 7th Cavalry, under Captain Owen Hale, followed Miles’ plan by continuing a rapid advance on the village. As they approached, a group of Nez Perce rose up from a coulee and opened fire, killing and wounding several soldiers. The soldiers fell back. Miles ordered two of the three companies in the 7th cavalry to dismount and quickly brought up the mounted infantry, the 5th, to join them in the firing line. Company K meanwhile had become separated from the main force and was also taking casualties. By 3 p.m. Miles had his entire force organized and on the battlefield and he occupied the higher ground. The Nez Perce were surrounded and had lost all their horses. Miles ordered a charge on the Nez Perce positions with the 7th Cavalry and one company of the infantry, but it was beaten back with heavy casualties.

At nightfall on September 30, Miles’ casualties amounted to 18 dead and 48 wounded, including two wounded Indian scouts. The 7th Cavalry took the heaviest losses. Its 110 men suffered 16 dead and 29 wounded, two of them mortally. The Nez Perce had 22 men killed, including three leaders: Joseph’s brother Ollokot, Toohoolhoolzote, and Poker Joe – the last killed by a Nez Perce sharpshooter who mistook him for a Cheyenne.^[23] Several Nez Perce women and children had also been killed.

Miles said of the battle that "The fight was the most fierce of any Indian engagement I have ever been in....The whole Nez Perce movement is unequalled in the history of Indian warfare."^[24]

During the cold and snowy night following the battle both the Nez Perce and the soldiers fortified their positions. Some Nez Perce crept out between the lines to collect ammunition from wounded and dead soldiers. ^[25] The Nez Perce dug large and deep shelter pits for women and children and rifle pits for the warriors covering all approaches to their camp which was a square about 250 yards (220 mts) on each side. About 100 warriors manned the defenses, each armed with three guns including a repeating rifle.^[26] In the words of a soldier: “to charge them would be madness.^[27]

Miles greatest fear – and the Nez Perce’s greatest hope – was that Sitting Bull might send Lakota warriors south from Canada to rescue the Nez Perce. The next morning, the soldiers saw what they thought were mounted columns of Indians on the horizon, but they turned out to be herds of bison. Looking Glass was killed at some point during the siege, when he thought he saw an approaching Lakota and raised his head above a rock to see better and was hit and killed instantly by a sniper’s bullet. ^[28]

The Cheyenne scouts may have initiated negotiations. Three of them rode into the Nez Perce fortifications and proposed talks with Miles. When Miles agreed, Chief Joseph and five other Nez Perce, including Tom Hill, of mixed Nez Perce\Delaware heritage who acted as interpreter. Soldiers and warriors collected the bodies of their dead during the truce. When the negotiations were unsuccessful, Miles apparently took Joseph prisoner. According to a Nez Perce warrior, Yellow Wolf, “Joseph was hobbled hands and feet” and rolled up in a blanket.^[29] Miles’ violation of the truce, however, was checkmated by the Nez Perce. A young lieutenant named Lovell H. Jerome wandered “through his own folly” into the Nez Perce camp during the truce. The Nez Perce took Jerome hostage and the next day, October 2, an exchange of Chief Joseph for Jerome was carried out.^[30]

On October 3, the soldiers opened fire again with a 12-pounder Napoleon gun which did little damage to the dug-in Nez Perce although one woman and one small girl were killed when a shell hit a shelter pit. On October 4, in the evening, General Howard with an escort arrived at the battlefield. Howard generously allowed Miles to retain tactical control of the siege.^[31]

Meanwhile, the Nez Perce were divided on the subject of surrender, Joseph apparently in favor while White Bird, the one other surviving leader, opposed surrender and favored a break-out through the army’s lines and a dash toward Canada. Joseph later said, “We could have escaped from Bear Paw Mountain if we had left our wounded, old women, and children behind. We were unwilling to do this. We had never heard of a wounded Indian recovering while in the hands of white men.”^[32]


In 1879 Chief Joseph went to Washington, D.C. to meet with President Rutherford B. Hayes and plead the case of his people. In 1885, Chief Joseph and his followers were allowed to return to the Pacific Northwest. Some of the Nez Perce were allowed to settle on the Nez Perce reservation around Kooskia, Idaho, but Joseph and others were taken to the Colville Indian Reservation far from both the rest of their people in Idaho and their homeland in the Wallowa Valley.

Colonel Nelson A. Miles gained the most benefit from his participation in the Nez Perce War. His success at Bear's Paw boosted his stock among the leading Indian-fighting officers of the army. In 1880, Miles won the rank of brigadier general commanding the Department of the Columbia, succeeding Howard in this assignment. Five years later, he took command of the Department of the Missouri, headquartered at Fort Leavenworth. In 1886, he supplanted General Crook in the campaign against the Chiricahua Apaches, finally forcing Geronimo's surrender. When Crook died in 1890, Miles moved to Chicago to command the Division of the Missouri, and in 1895, based on seniority, he became Commanding General of the Army. Yet Miles's astounding lack of strategic vision about how the army should change as it assumed new responsibilities in the world during and following the Spanish-American War, as well as his obstinate and increasingly outspoken disposition, rendered him expendable, and he retired in 1903. Largely forgotten in the years that followed, he collapsed and died in 1925, while attending a circus with his grandchildren in Washington, D.C.

Decades later, many Nez Perce men and women related their experiences with the army in 1877, adding significantly to the knowledge, but also to the perspective, of that history. Among them were Wottolen, the tribal historian (who lived to age 109), Two Moon, White Hawk, and Peopeo Tholekt, all participants in the battles and skirmishes. Over the course of almost three decades, Yellow Wolf, who as a young warrior had lived through the events, gave data to historian Lucullus V. McWhorter and accompanied him several times to the sites of the actions, including Big Hole and Bear's Paw. His reminiscences comprise a vital body of information essential to understanding the course of the struggle from Camas Prairie through Bear's Paw, Canada, the Indian Territory, and after. Yellow Wolf died at the Colville Reservation in 1935.[20]

The last Nez Perce survivor of the odyssey was Josiah Red Wolf, who had been but a child when the war took place. He passed away on March 23, 1971, at age ninety-nine.

NEZ PERCE SUMMER, 1877
The U.S. Army and the Nee-Me-Poo Crisis

420 (cannabis culture)

420, 4:20, or 4/20 (pronounced four-twenty) is a code-term used primarily in North America that refers to the consumption of cannabis and by extension, as a way to identify oneself with cannabis subculture or simply cannabis itself. Observances based on the number 420 include smoking cannabis around the time 4:20 p.m. (with some sources also indicating 4:20 a.m.^[1][2]), on any given day, as well as smoking cannabis on the date April 20 (4/20 in American form).^[3]

A widely discussed story says that a group of teenagers in San Rafael, California,^[4][5] calling themselves the Waldos,^[6] because, "their chosen hang-out spot was a wall outside the school",^[7] used the term in connection with a fall 1971 plan to search for an abandoned cannabis crop that they had learned about.^[6][8] The Waldos designated the Louis Pasteur statue on the grounds of San Rafael High School as their meeting place, and 4:20 p.m. as their meeting time.^[7] The Waldos referred to this plan with the phrase "4:20 Louis". Multiple failed attempts to find the crop eventually shortened their phrase to simply "4:20", which ultimately evolved into a codeword that the teens used to mean pot-smoking in general.^[8] Mike Edison says that Steve Hager of High Times was responsible for taking the story about the Waldos to "mind-boggling, cult like extremes" and "suppressing" all other stories about the origin of the term.^[9]
Hager wrote "Stoner Smart or Stoner Stupid?" in which he called for 4:20 p.m. to be the socially accepted hour of the day to consume cannabis.^[10] He attributes the early spread of the phrase to Grateful Dead followers, who were also linked to the city of San Rafael.^[10]

April 20 has become a counterculture holiday in North America, where people gather to celebrate and consume cannabis.^[2][3] Some events have a political nature to them, advocating for the legalization of cannabis. North American observances have been held in San Francisco's Golden Gate Park near the Haight-Ashbury district,^[11] the University of Colorado's Boulder campus,^[5][12][13] Ottawa, Ontario, at Parliament Hill and Major's Hill Park,^[14][15] Montréal, Québec at Mount Royal monument,^[16][17] Edmonton, Alberta at the Alberta Legislature Building,^[18] as well as Vancouver, British Columbia at the Vancouver Art Gallery.^[19] The growing size of the unofficial event at UC Santa Cruz caused the Vice Chancellor of Student Affairs to send an e-mail to parents in 2009 stating: "The growth in scale of this activity has become a concern for both the university and surrounding community."^[20]
Events have also occurred in Auckland, New Zealand at the Daktory.^{[21][unreliable source?]} and Dunedin, New Zealand, at University of Otago.^{[22][23][24][25][26][27]}

Persona

From Latin persōna (“mask; character”), sometimes said to derive from personare (“to sound through”) or from Etruscan 𐌘𐌄𐌓𐌔𐌖 (φersu), from Ancient Greek πρόσωπον (prosōpon).

persona (plural personas or personae or personæ)

1. A social role.
2. A character played by an actor.
3. (psychology) The mask or appearance one presents to the world.
4. (computing) A type of skin used in Mozilla software.

Education

Dolor de cabeza

PLANEAT

Dr T. Colin Campbell, Dr Caldwell B. Esselstyn Jr., and environmental scientist Professor Gidon Eshel are the heroes of the new award-winning documentary film PLANEAT, the story of these men’s search for a diet, which is good for our health, and good for the future of the planet. The film features an additional cast of pioneering chefs and some of the best plant-based cooking you have ever seen.


Click here to watch PLANEAT by streaming to your computer. A share of the proceeds from the film streaming will be donated to the T Colin Campbell Foundation.

Alan Watts - The Pathetic Fallacy

Published on May 21, 2012

If you can really understand this, then the seed of that radical revolution has already been planted
Change comes into being when there is no fear, when there is neither the experiencer nor the experience; it is only then that there is the revolution which is beyond time. But that cannot be as long as I am trying to change the 'I', as long as I am trying to change what is into something else. I am the result of all the social and the spiritual compulsions, persuasions, and all the conditioning based on acquisitiveness -my thinking is based on that. To be free from that conditioning, from that acquisitiveness, I say to myself, 'I must not be acquisitive; I must practice nonacquisitiveness.' But such action is still within the field of time, it is still the activity of the mind. Just see that. Don't say, 'How am I to get to that state when I am nonacquisitive?' That is not important. It is not important to be nonacquisitive; what is important is to understand that the mind which is trying to get away from one state to another is still functioning within the field of time, and therefore there is no revolution, there is no change. If you can really understand this, then the seed of that radical revolution has already been planted and that will operate: you have not a thing to do.

Jiddu Krishnamurti

Alan Watts - The Fool,The Joker And The Monk

Alan Watts ~ Living Life As A Bodhisattva

Ark

Uploaded on Jan 10, 2011
«Inspirado» en el calentamiento global y en el consiguiente aumento del nivel del mar, el arquitecto ruso Alexander Remizov ha realizado un proyecto de hotel totalmente sostenible.
Se llama «Ark» y ha sido ideado en colaboración con una empresa de ingeniería alemana y el científico moscovita Lev Britvin. Para su construcción se necesitarán madera, acero y plástico Etileno-TetraFluorEtileno.
La estructura ha sido diseñada con el objetivo de ser completamente autosuficiente gracias a un sistema de generadores de energía eólica y solar.

Este hotel flotante mediría cerca de 14.000 metros cuadrados y estaría pensado para albergar a 10.000 personas.
«Podría ser construido en sólo 3 o 4 meses y en cualquier parte del mundo» ha declarado Remizov, quien abrió su primer estudio en 1991.

xbetto2001 2 years ago

No se inspira en el calentamiento GLOBAL, mejor es decir " la idea nace por la preocupación alarmante del calentamiento global" , el diseño es muy idealista, me apena pero este diseño no cumple el menor estándar de ARQUITECTURA NAVAL, ha sido concebido como un edificio pensando que solo FLOTA en el agua tranquila. LA PERFORMANCE de una embarcación es una CIENCIA RIGUROSA , las imágenes de edificios por computadora son muy vendedoras pero muchas veces poco científicas

Human Bacteria

Human Bacteria Mapped; Gut Bacteria Linked To Happiness, Inflammatory Bowel Disease, Rheumatoid Arthritis, And Body Weight / Obesity

MONDAY, JUNE 18, 2012 AT 9:56AM

Campylobacter, a bacteria found in the human gut

Researchers recently completed an extensive, 5-year Human Microbiome Project (HMP)identifying more than 10,000 bacterial species living in and on our bodies.  The goal of HMP was to “map the normal microbial make-up of healthy humans.”[I]  Many believe the Human Microbiome Project will allow scientists and physicians to prevent and treat diseases in the future.  Researcher and pediatric gastroenterologist Dr. Phillip Tarr commented “This is really a new vista in biology.  This opens up many, many new opportunities to improve the health of our population.”

Coincidentally, the conclusion of the Human Microbiome Project coincided with the publication of several fascinating articles about gut bacteria and human health.[Ii]   For example, researchers recently linked gut bacteria with:

• Happiness 
• Inflammatory Bowel Disease
• Rheumatoid Arthritis
• Body weight / obesity

Happiness

Scientists at the University College Cork in Ireland recently discovered that an Absence Of Bacteria In Early Life May Decrease Levels Of Brain Serotonin later in life (serotonin is an important neurotransmitter implicated in depression).   This expounds upon previous research investigating potential Mind-Microbe Links.  

Inflammatory Bowel Disease (IBD)

Researchers also believe they may have identified why Western Diet Changes Gut Bacteria And May Trigger Immune-Mediated Diseases Like Inflammatory Bowel Disease (IBD).  Westernized countries tend to consume foods high in saturated fats, and researchers at the University of Chicago found that concentrated milk fats (common in processed foods and confectionary foods) alter the composition of bacteria in our digestive systems.  One bacteria in particular, Bilopha wadsworthia, thrives in the presence of saturated milk fats.  Interestingly, this same bacteria has been found in elevated levels in patients with inflammatory bowel conditions like IBD and appendicitis. 

Rheumatoid Arthritis

Researchers at the Mayo Clinic Linked Gut Bacteria To The Autoimmune Disease Rheumatoid Arthritis.  Rheumatoid arthritis is caused by the body’s immune system attacking its own tissue (like our joints). 

Through clever manipulation of genetic susceptibility to rheumatoid arthritis and introduction of different gut bacteria in mice, researchers concluded that gut bacteria may play an important role in developing rheumatoid arthritis and other autoimmune diseases like type I diabetes and multiple sclerosis (MS).  The researchers noted that changes related to aging (such as hormonal changes) may modulate gut bacteria and contribute to autoimmune disorders.   Specifically, the researchers believe autoimmune disorders may actually begin as an immune system attack on gut bacteria that have penetrated our intestinal walls. [Iii]

Body Weight / Obesity

Interestingly, researchers also recently summarized Evidence That Gut Bacteria Might Modify Body Weight.  Researchers at Arizona State University recently noted that bacteria play an important role in helping our body extract and synthesize important nutrients.  In fact, the body is unable to digest some carbohydrates without gut bacteria (the bacteria digest these carbs for us), and gut bacteria also produce important vitamins like biotin and folate and help us absorb other nutrients like magnesium, calcium, and iron. 

The researchers noted that obese individuals frequently have distinct gut bacteria.  For example, obese individuals typically have a greater proportion of bacteria from the phylum Bacteroidetes, while lean individuals have a greater proportion of bacteria from the phylulm Firmucutes.  Correlation does not imply causation.[Iv]  However, researchers are beginning to identify some compelling mechanisms by which gut bacteria may contribute to obesity.[V]  The researchers at Arizona State believe that we may be able to manipulate or exploit our gut bacteria in order to control weight. 

Future Implications

In an article titled Gut Check: Future Of Drugs May Rest With Your Microbes, Henry Haiser and Peter Tumbaugh of Harvard University note that “The trillions of microbes associated with the human body are a key part of a comprehensive view of pharmacology.”  In other words, future treatment of diseases (such as those noted above) and optimization of health will likely take into account our gut bacteria to a greater extent.  Once fairly obscure, gut bacteria (and the manipulation of gut bacteria) will likely play a greater role in maintaining health and preventing disease in the future. 

What Do You Think?

• Do you know of ways to optimize gut bacteria in order to optimize health?
• What role do you think gut bacteria will play in managing health and preventing disease in the future? 

Related:

• Irritable Bowel Syndrome (IBS) And Gut Bacteria Definitively Linked [vi]
• Additional relevant articles tagged 'Microorganisms' or 'Medicine'

---

[I] The human “microbiome” refers to microscopic bacteria, yeasts, protozoa, small parasitic worms, and viruses. However, most microbes in the human microbiome are bacteria; therefore, the terms human “microbiome” or “microbe” are often used to refer specifically to bacteria.    

[Ii] Note that most of our human microbiome resides in our gut.

[Iii] Gut bacteria typically do not penetrate the intestine’s walls and enter the body.  However, researchers believe that under certain conditions (such as certain hormonal conditions and other conditions related to aging), the gut bacteria may penetrate the intestinal wall stimulating an immune response that manifests as rheumatoid arthritis or possibly other autoimmune disease like type I diabetes or MS.  

[Iv] In other words, just because an increase in Bacteroidetes is correlated (or related) to an increase in body weight (obesity), this does not necessarily mean that an increase of Bacteroidetes causes obesity. 

[v] For example, researchers have noted that obesity and insulin-resistance (which could lead to Type II diabetes) are often accompanied by inflammation.  One marker of inflammation that has been associated with obesity and insulin-resistance is blood lipopolysaccharides (LPS).  Interestingly, LPS primarily comes from bacteria such as those that live in our gut. 

Additionally, scientists found that “germ free mice” (literally mice with no germs on or in them) experienced a 60% increase in body fat content and insulin resistance when gut bacteria from obese mice were transplanted to their guts.  Scientists also found that these same mice transplanted with gut bacteria from obese mice experienced a decreased production of a compound called Fiaf (“fasting-induced adipocyte factor).  Fiaf is produced in intestinal tissue and promotes leanness (in other words, opposes obesity).  Therefore, researchers believe that the gut bacteria of obese mice may suppress Fiaf production which in turn promotes obesity.

[vi] If you're curious, here's an excellent reference on the Difference Between Irritable Bowel Syndrome (IBS) And Inflammatory Bowel Disease (IBD)

Nutrition for Eyesight

• 
  

  "Eat your carrots" is good advice for your eyes. Carrots are loaded with beta-carotene, which converts to vitamin A and forms a purple pigment in the retina of the eye called rhodopsin, which is needed by the eye in order to see in dim light. If you don't get enough vitamin A or beta-carotene, your body cannot produce an adequate amount of rhodopsin. For this reason, many people end up with night blindness. The lack of beta-carotene is also attributed to macular degeneration.

  Plants and vegetables that are bright and colorful are often loaded with beta-carotene. Carrots, pumpkin, dark leafy green and sweet potatoes are all excellent sources.

  Lutein, a compound found in eye tissue, also aids in preventing macular degeneration. Sources of lutein include spinach, corn and leafy green vegetables. It is also available in over-the-counter supplements.

  Since free radicals can cause eye damage, eating foods that are rich in antioxidants only stands to reason. Eggs, onions, avocados and asparagus all contain an antioxidant called glutathione, which attacks free radicals and aids in cataract prevention.

  Other antioxidants that protect against free radicals are vitamin C and vitamin E. Found in fresh fruits and vegetables, vitamin C also protects against cataracts and clouding of the eyes. Foods with the highest vitamin C concentrations per serving are spinach, peppers, broccoli, brussels sprouts and citrus fruits. Vitamin E is difficult to obtain through diet only, but it is available in wheat germ, kale, sweet potatoes, avocados, almonds and blueberries. Vitamins C and E are readily available as dietary supplements, but obtaining them through diet is the preferred method for your body to utilize them.

  Healthy fats that contain omega-3 fatty acids benefit the eyes as well. They keep the blood vessels and nerves that go to the eyes healthy and young. Excellent food sources of omega-3s are sardines and salmon. Eating two to three portions a week is recommended, and daily dietary supplements also help.

What Not To Eat

• 
  

  Eating the best foods for your eyes can be sabotaged if you continue to include items in your diet that counteract their effects. Caffeine can deplete vitamins and minerals from your body, including the ones necessary for eye health.

  Foods that are high in preservatives or highly processed also deplete vitamin stores, and are also known to cause inflammation. Inflammation increases pressure around the nerves and blood vessels that go to the eyes, causing poor vision and not allowing proper blood flow to deliver necessary vitamins and minerals to the tissues.

  Free radicals in our bodies are increased by poor lifestyle choices, such as smoking and stress, and other factors such as pollution. Try as much as you can to limit your exposure to these things as you add the above healthy foods to your diet.

Read more: How Does Diet Affect Eyesight? | eHow.com http://www.ehow.com/how-does_4742978_diet-affect-eyesight.html#ixzz1WxmEQjfd