The Myth of Big, Bad Gluten

来源: https://www.nytimes.com/2015/07/05/opinion/sunday/the-myth-of-big-bad-gluten.html


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[1] AS many as one in three Americans tries to avoid gluten, a protein found in wheat, barley and rye. Gluten-free menus, gluten-free labels and gluten-free guests at summer dinners have proliferated.

[2] Some of the anti-glutenists argue that we haven’t eaten wheat for long enough to adapt to it as a species. Agriculture began just 12,000 years ago, not enough time for our bodies, which evolved over millions of years, primarily in Africa, to adjust. According to this theory, we’re intrinsically hunter-gatherers, not bread-eaters. If exposed to gluten, some of us will develop celiac disease or gluten intolerance, or we’ll simply feel lousy.

[3] Most of these assertions, however, are contradicted by significant evidence, and distract us from our actual problem: an immune system that has become overly sensitive.

[4] Wheat was first domesticated in southeastern Anatolia perhaps 11,000 years ago. (An archaeological site in Israel, called Ohalo II, indicates that people have eaten wild grains, like barley and wheat, for much longer — about 23,000 years.)

[5] Is this enough time to adapt? To answer that question, consider how some populations have adapted to milk consumption. We can digest lactose, a sugar in milk, as infants, but many stop producing the enzyme that breaks it down — called lactase — in adulthood. For these “lactose intolerant” people, drinking milk can cause bloating and diarrhea. To cope, milk-drinking populations have evolved a trait called “lactase persistence”: the lactase gene stays active into adulthood, allowing them to digest milk.

[6] Milk-producing animals were first domesticated about the same time as wheat in the Middle East. As the custom of dairying spread, so did lactase persistence. What surprises scientists today, though, is just how recently, and how completely, that trait has spread in some populations. Few Scandinavian hunter-gatherers living 5,400 years ago had lactase persistence genes, for example. Today, most Scandinavians do.

[7] Here’s the lesson: Adaptation to a new food stuff can occur quickly — in a few millenniums in this case. So if it happened with milk, why not with wheat?

[8] “If eating wheat was so bad for us, it’s hard to imagine that populations that ate it would have tolerated it for 10,000 years,” Sarah A. Tishkoff, a geneticist at the University of Pennsylvania who studies lactase persistence, told me.

[9] For Dr. Bana Jabri, director of research at the University of Chicago Celiac Disease Center, it’s the genetics of celiac disease that contradict the argument that wheat is intrinsically toxic.

[10] Active celiac disease can cause severe health problems, from stunting and osteoporosis to miscarriage. It strikes a relatively small number of people — just around 1 percent of the population. Yet given the significant costs to fitness, you’d anticipate that the genes associated with celiac would be gradually removed from the gene pool of those eating wheat.

[11] A few years ago, Dr. Jabri and the population geneticist Luis B. Barreiro tested that assumption and discovered precisely the opposite. Not only were celiac-associated genes abundant in the Middle Eastern populations whose ancestors first domesticated wheat; some celiac-linked variants showed evidence of having spread in recent millenniums.

[12] People who had them, in other words, had some advantage compared with those who didn’t.

[13] Dr. Barreiro, who’s at the University of Montreal, has observed this pattern in many genes associated with autoimmune disorders. They’ve become more common in recent millenniums, not less. As population density increased with farming, and as settled living and animal domestication intensified exposure to pathogens, these genes, which amp up aspects of the immune response, helped people survive, he thinks.

[14] In essence, humanity’s growing filth selected for genes that increase the risk of autoimmune disease, because those genes helped defend against deadly pathogens. Our own pestilence has shaped our genome.

[15] The benefits of having these genes (survival) may have outweighed their costs (autoimmune disease). So it is with the sickle cell trait: Having one copy protects against cerebral malaria, another plague of settled living; having two leads to congenital anemia.

[16] But there’s another possibility: Maybe these genes don’t always cause quite as much autoimmune disease.

[17] Perhaps the best support for this idea comes from a place called Karelia. It’s bisected by the Finno-Russian border. Celiac-associated genes are similarly prevalent on both sides of the border; both populations eat similar amounts of wheat. But celiac disease is almost five times as common on the Finnish side compared with the Russian. The same holds for other immune-mediated diseases, including Type 1 diabetes, allergies and asthma. All occur more frequently in Finland than in Russia.

[18] WHAT’S the difference? The Russian side is poorer; fecal-oral infections are more common. Russian Karelia, some Finns say, resembles Finland 50 years ago. Evidently, in that environment, these disease-associated genesdon’t carry the same liability.

[19] Are the gluten haters correct that modern wheat varietals contain more gluten than past cultivars, making them more toxic? Unlikely, according to recent analysis by Donald D. Kasarda, a scientist with the United States Department of Agriculture. He analyzed records of protein content in wheat harvests going back nearly a century. It hasn’t changed.

[20] Do we eat more wheat these days? Wheat consumption has, in fact, increased since the 1970s, according to the U.S.D.A. But that followed an earlier decline. In the late 19th century, Americans consumed nearly twice as much wheat per capita as we do today.

[21] We don’t really know the prevalence of celiac disease back then, of course. But analysis of serum stored since the mid-20th century suggests that the disease was roughly one-fourth as prevalent just 60 years ago. And at that point, Americans ate about as much wheat as we do now.

[22] Overlooked in all this gluten-blaming is the following: Our default response to gluten, says Dr. Jabri, is to treat it as the harmless protein it is — to not respond.

[23] So the real mystery of celiac disease is what breaks that tolerance, and whatever that agent is, why has it become more common in recent decades?

[24] An important clue comes from the fact that other disorders of immune dysfunction have also increased. We’re more sensitive to pollens (hay fever), our own microbes (inflammatory bowel disease) and our own tissues (multiple sclerosis).

[25] Perhaps the sugary, greasy Western diet — increasingly recognized as pro-inflammatory — is partly responsible. Maybe shifts in our intestinal microbial communities, driven by antibiotics and hygiene, have contributed. Whatever the eventual answer, just-so stories about what we evolved eating, and what that means, blind us to this bigger, and really much more worrisome, problem: The modern immune system appears to have gone on the fritz.

[26] Maybe we should stop asking what’s wrong with wheat, and begin asking what’s wrong with us.


myth noun (许多人相信的)错误观念
[ C + that ] disapproving a commonly believed but false idea
barley /ˈbɑː.li/ noun [ U ] 大麦
rye /raɪ/ noun [ U ] 黑麦
proliferate /prəˈlɪf. ə r.eɪt/ verb [ I ] formal
to increase a lot and suddenly in number
species /ˈspiː.ʃiːz/ noun [ C ] plural species 物种
adjust /əˈdʒʌst/ verb
[ I ] to become more familiar with a new situation
intrinsically /ɪnˈtrɪn.zɪ.kli/ adv 在本质上
hunter-gatherer 采猎者(以打猎和采集植物为生的人)
celiac disease 乳糜泻
intolerance /ɪnˈtɒl. ə r. ə n t  s/ noun (对食物或药物的)过敏,不耐受
[ C or U ] If you have a food intolerance, you cannot digest a particular food in a normal way and may feel ill if you eat it
lousy /ˈlaʊ.zi/ adj informal very bad
assertion /əˈsɜː.ʃ ə n/ noun [ C + that ] 论断
a statement that you strongly believe is true
contradict /ˌkɒn.trəˈdɪkt/ verb [ I or T ] 驳斥;与……相抵触
distract /dɪˈstrækt/ verb [ T ] 分散(注意力)
to make someone stop giving their attention to something
immune system 免疫系统
overly /ˈəʊ.v ə l.i/ adverb ( also over ) too; very

domesticate /dəˈmes.tɪ.keɪt/ verb [ T often passive ]
to bring animals or plants under human control in order to provide food, power or companionship
Anatolia 安纳托利亚
archaeological , US also archeological /ˌɑː.ki.əˈlɒdʒ.ɪ.k ə l/ adj 考古学上的
Israel 以色列
lactose /ˈlæk.təʊs/ noun [ U ] specialized
a type of sugar which is found in milk
lactase 乳糖分解孝素
bloat /bləʊt/ / verb [ I or T ] 使膨胀;膨胀
diarrhoea , mainly US diarrhea /ˌdaɪ.əˈriː.ə/ noun [ U ] 腹泻
an illness in which the body's solid waste is more liquid than usual and comes out of the body more often
cope /kəʊp/ verb [ I ]
to deal successfully with a difficult situation
trait /treɪt/ noun [ C ] 特性
lactase persistence 乳糖耐受性
dairying 乳品制造业
Scandinavian 斯堪的纳维亚人
millennium /mɪˈlen.i.əm/ noun [ C ] plural millennia or millenniums
a period of 1000 years, or the time when a period of 1000 years ends
genetics /dʒəˈnet.ɪks/ /-ˈnet ̬-/ noun [ U ] 遗传学
stunt /stʌnt/ verb [ T ] 抑制成长发育
to prevent the growth or development of something from reaching its limit
osteoporosis /ˌɒs.ti.əʊ.pəˈrəʊ.sɪs/ noun [ U ] 骨质疏松症
a disease which causes the bones to become weaker and easily broken
miscarriage /ˈmɪsˌkær.ɪdʒ/ /-ˌker-/ noun [ C or U ] 流产
given /ˈgɪv. ə n/ prep
knowing about or considering a particular thing
gene ˌ pool noun [ C ] 基因库
all the genes of a particular group of people or animals
variant /ˈveə.ri.ənt/ /ˈver.i-/ noun [ C ] 变异体
auto-immune /ˌɔː.təʊ.ɪˈmjuːn/ adj [ before noun ] specialized 自身免疫的
pathogen /ˈpæθ.ə.dʒən/ noun [ C ] 病原体
amp up 放大
in essence formal 本质上
relating to the most important characteristics or ideas of something
deadly /ˈded.li/ adj likely to cause death 致命的
pestilence /ˈpes.tɪ.ləns/ noun 瘟疫
genome /ˈdʒiː.nəʊm/ / noun [ C ] specialized 基因组
outweigh /ˌaʊtˈweɪ/ verb [ T ]
to be greater or more important than something else
sickle cell 镰状细胞
cerebral malaria 脑型疟疾
plague /pleɪg/ noun [ C or U ] 瘟疫
congenital /kənˈdʒen.ɪ.t ə l/ adj 天生的
anemia /əˈniː.mi.ə/ noun [ U ] mainly US for anaemia 贫血
bisect /baɪˈsekt/ verb [ T ]
to divide something into two, usually equal, parts
immune-mediated 免疫介导的
asthma /ˈæs.mə/ noun [ U ] 哮喘
fecal-oral 粪-口(接触排泄物)
liability /ˌlaɪ.əˈbɪl.ɪ.ti/ /-ə.t ̬i/ noun 职责
varietal 品种
cultivar 品种
serum stored 血清存储
default /dɪˈfɒlt/ noun 系统默认值
disorder /dɪˈsɔː.də r / noun
[ C or U ] an illness of the mind or body
dysfunction /dɪsˈfʌŋk.ʃ ə n/ noun [ C ] specialized
a problem or fault in a part of the body or a machine
hay fever 花粉病
microbe /ˈmaɪ.krəʊb/ noun [ C ] 微生物
inflammatory bowel disease 炎症性肠病
tissue /ˈtɪʃ.uː/ noun [ U ] 组织
multiple sclerosis 多发性硬化(症)
greasy /ˈgriː.si/ adj
covered with or full of fat or oil
pro-inflammatory 促进炎症的
intestinal /ɪnˈtes.tɪ.nəl/ adj 肠道的
microbial communities 微生物群落
antibiotic /ˌæn.ti.baɪˈɒt.ɪk/ noun [ C or U ] 抗生素
hygiene /ˈhaɪ.dʒiːn/ noun [ U ] 卫生
just-so stories 这样的故事
go on the fritz 出现故障

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来源: https://www.nytimes.com/2015/07/05/opinion/sunday/the-myth-of-big-bad-gluten.html


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[1] AS many as one in three Americans tries to avoid gluten, a protein found in wheat, barley and rye. Gluten-free menus, gluten-free labels and gluten-free guests at summer dinners have proliferated.

[2] Some of the anti-glutenists argue that we haven’t eaten wheat for long enough to adapt to it as a species. Agriculture began just 12,000 years ago, not enough time for our bodies, which evolved over millions of years, primarily in Africa, to adjust. According to this theory, we’re intrinsically hunter-gatherers, not bread-eaters. If exposed to gluten, some of us will develop celiac disease or gluten intolerance, or we’ll simply feel lousy.

[3] Most of these assertions, however, are contradicted by significant evidence, and distract us from our actual problem: an immune system that has become overly sensitive.

[4] Wheat was first domesticated in southeastern Anatolia perhaps 11,000 years ago. (An archaeological site in Israel, called Ohalo II, indicates that people have eaten wild grains, like barley and wheat, for much longer — about 23,000 years.)

[5] Is this enough time to adapt? To answer that question, consider how some populations have adapted to milk consumption. We can digest lactose, a sugar in milk, as infants, but many stop producing the enzyme that breaks it down — called lactase — in adulthood. For these “lactose intolerant” people, drinking milk can cause bloating and diarrhea. To cope, milk-drinking populations have evolved a trait called “lactase persistence”: the lactase gene stays active into adulthood, allowing them to digest milk.

[6] Milk-producing animals were first domesticated about the same time as wheat in the Middle East. As the custom of dairying spread, so did lactase persistence. What surprises scientists today, though, is just how recently, and how completely, that trait has spread in some populations. Few Scandinavian hunter-gatherers living 5,400 years ago had lactase persistence genes, for example. Today, most Scandinavians do.

[7] Here’s the lesson: Adaptation to a new food stuff can occur quickly — in a few millenniums in this case. So if it happened with milk, why not with wheat?

[8] “If eating wheat was so bad for us, it’s hard to imagine that populations that ate it would have tolerated it for 10,000 years,” Sarah A. Tishkoff, a geneticist at the University of Pennsylvania who studies lactase persistence, told me.

[9] For Dr. Bana Jabri, director of research at the University of Chicago Celiac Disease Center, it’s the genetics of celiac disease that contradict the argument that wheat is intrinsically toxic.

[10] Active celiac disease can cause severe health problems, from stunting and osteoporosis to miscarriage. It strikes a relatively small number of people — just around 1 percent of the population. Yet given the significant costs to fitness, you’d anticipate that the genes associated with celiac would be gradually removed from the gene pool of those eating wheat.

[11] A few years ago, Dr. Jabri and the population geneticist Luis B. Barreiro tested that assumption and discovered precisely the opposite. Not only were celiac-associated genes abundant in the Middle Eastern populations whose ancestors first domesticated wheat; some celiac-linked variants showed evidence of having spread in recent millenniums.

[12] People who had them, in other words, had some advantage compared with those who didn’t.

[13] Dr. Barreiro, who’s at the University of Montreal, has observed this pattern in many genes associated with autoimmune disorders. They’ve become more common in recent millenniums, not less. As population density increased with farming, and as settled living and animal domestication intensified exposure to pathogens, these genes, which amp up aspects of the immune response, helped people survive, he thinks.

[14] In essence, humanity’s growing filth selected for genes that increase the risk of autoimmune disease, because those genes helped defend against deadly pathogens. Our own pestilence has shaped our genome.

[15] The benefits of having these genes (survival) may have outweighed their costs (autoimmune disease). So it is with the sickle cell trait: Having one copy protects against cerebral malaria, another plague of settled living; having two leads to congenital anemia.

[16] But there’s another possibility: Maybe these genes don’t always cause quite as much autoimmune disease.

[17] Perhaps the best support for this idea comes from a place called Karelia. It’s bisected by the Finno-Russian border. Celiac-associated genes are similarly prevalent on both sides of the border; both populations eat similar amounts of wheat. But celiac disease is almost five times as common on the Finnish side compared with the Russian. The same holds for other immune-mediated diseases, including Type 1 diabetes, allergies and asthma. All occur more frequently in Finland than in Russia.

[18] WHAT’S the difference? The Russian side is poorer; fecal-oral infections are more common. Russian Karelia, some Finns say, resembles Finland 50 years ago. Evidently, in that environment, these disease-associated genesdon’t carry the same liability.

[19] Are the gluten haters correct that modern wheat varietals contain more gluten than past cultivars, making them more toxic? Unlikely, according to recent analysis by Donald D. Kasarda, a scientist with the United States Department of Agriculture. He analyzed records of protein content in wheat harvests going back nearly a century. It hasn’t changed.

[20] Do we eat more wheat these days? Wheat consumption has, in fact, increased since the 1970s, according to the U.S.D.A. But that followed an earlier decline. In the late 19th century, Americans consumed nearly twice as much wheat per capita as we do today.

[21] We don’t really know the prevalence of celiac disease back then, of course. But analysis of serum stored since the mid-20th century suggests that the disease was roughly one-fourth as prevalent just 60 years ago. And at that point, Americans ate about as much wheat as we do now.

[22] Overlooked in all this gluten-blaming is the following: Our default response to gluten, says Dr. Jabri, is to treat it as the harmless protein it is — to not respond.

[23] So the real mystery of celiac disease is what breaks that tolerance, and whatever that agent is, why has it become more common in recent decades?

[24] An important clue comes from the fact that other disorders of immune dysfunction have also increased. We’re more sensitive to pollens (hay fever), our own microbes (inflammatory bowel disease) and our own tissues (multiple sclerosis).

[25] Perhaps the sugary, greasy Western diet — increasingly recognized as pro-inflammatory — is partly responsible. Maybe shifts in our intestinal microbial communities, driven by antibiotics and hygiene, have contributed. Whatever the eventual answer, just-so stories about what we evolved eating, and what that means, blind us to this bigger, and really much more worrisome, problem: The modern immune system appears to have gone on the fritz.

[26] Maybe we should stop asking what’s wrong with wheat, and begin asking what’s wrong with us.

下载PDF版