{"id":172,"date":"2013-11-12T18:11:19","date_gmt":"2013-11-12T18:11:19","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=172"},"modified":"2014-04-23T23:10:22","modified_gmt":"2014-04-23T23:10:22","slug":"molecules-in-the-blood-that-signal-self-destruction","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/","title":{"rendered":"Molecules in the Blood that Signal Self-Destruction"},"content":{"rendered":"

My theme the last few weeks has been the signals that trigger the body\u2019s self-destruction with age. \u00a0The easiest to target are molecules that circulate in the blood. \u00a0Last week, I covered a few that decrease in blood concentration as we age, and that cripple our defenses. \u00a0This week, I\u2019ll talk about signals that increase as we age, and that activate self-destruction. \u00a0There are two principal mechanisms of active self-destruction: \u00a0inflammation and apoptosis=cell suicide. \u00a0Both mechanisms are important to the healthy functioning of the body. \u00a0Inflammation is our first defense against invading pathogens. \u00a0Apoptosis elimnates diseased and cancerous cells before they can become a problem. \u00a0But in old age, both are co-opted for self-destruction. \u00a0Healthy tissues in the body are destroyed by apoptosis, and inflammation leads to arterial damage and heart disease, DNA damage and cancer. \u00a0<\/em><\/p>\n

The blood signals, too, are have helpful roles earlier in life, but turn traitorous with age.<\/em><\/p>\n

Two weeks ago, I listed some protective hormones that are down-regulated with age. \u00a0In this column, I review some hormones and other signals in the blood that rise with age, and contribute to weakness, loss of function and the diseases of old age.<\/p>\n

 <\/p>\n

NFk<\/span>B<\/strong><\/p>\n

The pro-inflammatory hormone NFk<\/span>B was first recognized in the 1940s<\/a>\u00a0as a risk factor for cancer.\u00a0 Circulating NFk<\/span>B increases with age, and it is hard to imagine any benefit to the body from this increase. \u00a0Last May, the laboratory of Dongsheng Cai<\/a>\u00a0at Einstein Med School reported<\/a>\u00a0that NFk<\/span>B is secreted by the hypothalamus \u2014 a tiny endocrine gland embedded within the brain, which is known as the clock that controls the daily rhythm of wake\/sleep cycles. \u00a0(More speculatively, the hypothalamus also controls the timing of development and, by extension, aging as well.) \u00a0Cai was able to shorten life span in mice with extra NFk<\/span>B, and to lengthen life span (10% increase in maximum life span) by inhibiting Nk<\/span>B.<\/p>\n

One of the least-understood aspects of ageing is its coordinated and stereotyped progression in all organ systems. Although researchers have long suspected that the brain orchestrates systemic ageing, compelling evidence of this in mammals has been lacking. Furthermore, we have had no clear understanding of how ageing is affected by inflammation, which is a hallmark of age-related diseases such as diabetes, cardiovascular disease, arthritis and Alzheimer’s disease. In this issue, Zhang et al.1<\/a> (page 211<\/a>) help to make this connection by documenting the integration of inflammatory responses with systemic control of ageing by the hypothalamus \u2014 a part of the brain that controls growth, reproduction and metabolism*<\/a>. \u00a0[<\/em>Ref<\/a>]<\/em><\/p>\n

 <\/p><\/blockquote>\n

\u00a0P-Smad3<\/strong><\/p>\n

Smad proteins are circulating transcription factors. \u00a0In other words, they are a way that a central command in the body can send a signal through the blood and affect which proteins are transcribed from DNA and manufactured in the peripheral cell.<\/p>\n

Smad3 affects creation of new cells which is necessary not just for healing but for keeping muscles healthy and strong. \u00a0Stem cells in the muscles are called satellite cells<\/a>, and these are activated every time we exercise to renew and strengthen the muscles.<\/p>\n

In aging muscle cells, P-Smad3 increases and holds back the cells\u2019 regenerative power. \u00a0In vitro studies show that satellite cells can be rejuvenated by reducing P-Smad3. \u00a0[Ref<\/a>]<\/p>\n

 <\/p>\n

Wnt<\/strong><\/p>\n

Wnt is a signal from outside of the cell that affects gene transcription inside the cell nucleus, and thus has a powerful, general effect initiated from the outside. \u00a0It\u2019s not a single protein, but many that effect signaling by the same pathway, with different results. \u00a0(cancer and insulin resistance fr overexpression\u2026) \u00a0Wnt is\u00a0overexpressed in cancer cells<\/a><\/p>\n

One of the most dynamic and innovative aging labs in the world is run by Irina and Michael Conboy at UC Berkeley. \u00a0I have\u00a0previously cited them<\/a>\u00a0in connection with parabiosis experiments. \u00a0The Conboys\u00a0reported back in 2007<\/a>\u00a0that Wnt signaling changes with age (in mice) in ways that inhibit healing and muscle regeneration. \u00a0 Unfortunately, it\u2019s not as simple as \u201ctoo much Wnt\u201d, because Wnt is not a single hormone but a whole family of signals. [follow-up ref<\/a>; \u00a0another ref<\/a>]<\/p>\n

 <\/p>\n

TGF-\u03b2
\n<\/strong><\/p>\n

T<\/strong>ransforming G<\/strong>rowth F<\/strong>actor-beta proteins are multifunctional cytokines<\/a> (fancy name for a signaling molecule), secreted by numerous cell types. They are capable of signaling to virtually every cell type and broadly control cell proliferation, differentiation, apoptosis, inflammation and scarring in various tissues [Ref<\/a>]. \u00a0TGF-\u03b2 may contribute to too much apoptosis and too little stem activity as we age. \u00a0The Conboy lab, writing about TGF-\u03b2 and Wnt:<\/p>\n

The results shown here argue against the notion of systemic TGF-\u03b21 endocrine activity and strongly suggest that TGF-\u03b2, released by the known process of platelet activation during sera collection, inhibits satellite cell responses in vitro. These findings also suggest that young sera may contain a functional and natural decoy of TGF-\u03b21, or a competitor of TGF-\u03b21 signaling pathway (either endocrine or released by platelets). Lastly, our results demonstrate that Wnt antagonizes, rather than synergizes with TGF-\u03b21-mediated satellite cell response inhibition.\u00a0[<\/em>Ref<\/a>]<\/em><\/p><\/blockquote>\n

 <\/p>\n

\u2026in other words, we have more TGF-\u03b2 as we get older, and its activity is inhibited when we are younger. TGF-\u03b2 plays a role in inactivating stem cells, which we need for repair and rebuilding.<\/p>\n

LH and FSH<\/strong><\/p>\n

L<\/strong>uteinizing H<\/strong>ormone and F<\/strong>ollicle-S<\/strong>timulating H<\/strong>ormone have their best-known role in the female menstrual cycle. \u00a0Men have much less than women at all ages. \u00a0But surprisingly, both these \u201cgonadotropins\u201d increase with age<\/a>. \u00a0What are women doing with extra menstrual hormones after they stop menstruating? \u00a0In fact it is now accepted that high levels of FSH are programmed from the pituitary (brain) as women approach menopause, and that FSH is part of the hormonal signal that initiates menopause<\/a>.<\/p>\n

Back in 1998, Jeff Bowles published<\/a> an evolutionary hypothesis\u00a0that LH and FSH were signals that induce aging and purposefully increase mortality in both men and women. \u00a0Remarkably, a good deal of circumstantial evidence has accumulated since that time in support of Bowles\u2019s idea.<\/p>\n

Female mice that overexpress FSH receptor age prematurely. [Ref<\/a>]<\/p>\n

In women, high FSH is associated with bone loss and osteoporosis<\/a>, and also with growth of fat cells<\/a>\u00a0and weight gain.<\/p>\n

\u00a0In men, high FSH is associated with enlarged prostate and with prostate cancer<\/a>. \u00a0(The prostate is one source, secreting FSH.) \u00a0High (age-adjusted) FSH is associated with an increase in all-cause mortality in men<\/a>. \u00a0In middle-aged males, high FSH is associated with muscle pain<\/a>\u00a0and increased frailty<\/a>.<\/p>\n

There is a literature of antibodies against the gonadotropins<\/em> (LH and FSH) going back at least to 1934. \u00a0Anti-gonadotropins are used to treat sex-associated cancers<\/a>, and here<\/a> is a clinical trial that is trying antigonadotropins as an Alzheimer treatment. \u00a0I am not aware of anti-aging therapies based on blocking the action of FSH and LH, but this would not be difficult to accomplish, and I think the experiment is well worth trying.<\/p>\n

Cortisol<\/strong><\/p>\n

Cortisol<\/a> is the opposite of inflam-aging. \u00a0Cortisol damps the body’s immune response, making it more tolerant. \u00a0And yet, cortisol increases as we age (more in women than men<\/a>), and there are reasons to believe that the results are not good for us.<\/p>\n

Cortisol provides the trigger that causes the Pacific salmon’s body to self-destruct after it has returned to fresh water and spawned. \u00a0Cortisol increases sugar in the blood, part of the insulin resistance of metabolic syndrome<\/a>. \u00a0Cortisol levels rise with chronic stress. \u00a0Cortisol is associated with age-related memory decline<\/a>, with depression and dementia<\/a>.<\/p>\n

Cushing’s Syndrome<\/a> is the name given to a constellation of symptoms associated with over-exposure to cortisol, and many of these symptoms sound like “normal aging”: thinning of the skin, rubber tire around the waist, sleep disorders, baldness in men, high blood pressure and a tendency toward osteoporosis.<\/p>\n

Drugs that block cortisol receptors<\/a> are known, but are not in common use.<\/p>\n

p53<\/strong><\/p>\n

P53 promotes apoptosis, which is programmed cell death. \u00a0It is important for eliminating diseased cells and suppressing cancer. \u00a0But as we age, we have too much p53, and many non-cancerous cells begin to commit suicide, with the result that we lose healthy tissue in the muscles and, even more important, neurons in the brain.<\/p>\n

P53 does not circulate in the blood, and in this sense does not belong in the present list. \u00a0It is produced endogenously in each cell. \u00a0The amount of p53 (and most other proteins) is regulated by a balance between transcription and degradation. \u00a0Transcription is the process of reading a DNA gene into messenger RNA, which travels to a ribosome, where its instructions are translated, 3 by 3, into a sequence of amino acids that makes a unique protein. \u00a0Degradation is managed by first tagging of proteins targeted for destruction using the label molecule ubiquitin<\/a>. \u00a0A protein with several ubiquitin tags is recognized by the cell and dragged to the nearest proteosome<\/a> for recycling.<\/p>\n

In unstressed cells, p53 levels are kept low through a continuous degradation of p53. A protein called\u00a0Mdm2<\/a>\u00a0(also called HDM2 in humans), which is itself a product of p53, binds to p53, preventing its action and transports it from the\u00a0nucleus<\/a>\u00a0to the\u00a0cytosol<\/a>. Also Mdm2 acts as\u00a0ubiquitin ligase<\/a>\u00a0and covalently attaches\u00a0ubiquitin<\/a>\u00a0to p53 and thus marks p53 for degradation by the\u00a0proteasome<\/a>. However, ubiquitylation of p53 is reversible. [hfrom Armando Rivera-Malo in Google Books<\/a>]<\/p><\/blockquote>\n

If there is too much p53 late in life, this is executed at the level of the cell, but it happens in response to (yet unidentified) blood-borne signals that carry directives from the brain.<\/p>\n

 <\/p>\n

Homocysteine<\/strong><\/p>\n

Homocysteine is a variant of an amino acid used as a basic protein building block. \u00a0It is a small molecule. \u00a0Increased amounts of homocysteine in the blood are a risk factor for CV disease. \u00a0Folic acid (a B vitamin) can reduce homocysteine in the blood<\/a>. \u00a0But whether the association is causal is controversial [Ref – No<\/a>;\u00a0\u00a0Ref – Yes<\/a>]<\/p>\n

Homocysteine\u2019s health risks are thought to come from deterioration of endothelial cells in the linings of blood vessels. \u00a0This damage can be reduced by dietary supplementation with curcumin<\/a> (the anti-inflammatory agent in the Indian spice-root turmeric).<\/p>\n

 <\/p>\n

Sex hormones<\/strong><\/p>\n

Sex hormones decline with age. \u00a0There is a lot of data on hormone replacement therapy in women (estrogen and progesterone), and less but also considerable data on testosterone replacement in aging men. \u00a0Different studies produce different results, and interpretations are contentious. \u00a0Are sex hormones a mortality risk, or a protection? \u00a0This is a big topic, and I\u2019m going to have to defer it to another day.<\/p>\n

The Bottom Line<\/strong><\/p>\n

There are several known blood signals that promote age-related destruction and disease, and probably many more that are not yet known. \u00a0Already we know enough to be able to target these signals with anti-bodies and other molecules that block their action. \u00a0What are we waiting for?<\/p>\n","protected":false},"excerpt":{"rendered":"

My theme the last few weeks has been the signals that trigger the body\u2019s self-destruction with age. \u00a0The easiest to target are molecules that circulate in the blood. \u00a0Last week, I covered a few that decrease in blood concentration as we age, and that cripple our defenses. \u00a0This week, I\u2019ll talk about signals that increase … Read more<\/a><\/p>\n","protected":false},"author":65,"featured_media":0,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"_jetpack_newsletter_access":"","_jetpack_dont_email_post_to_subs":false,"_jetpack_newsletter_tier_id":0,"_jetpack_memberships_contains_paywalled_content":false,"_jetpack_memberships_contains_paid_content":false,"footnotes":"","jetpack_post_was_ever_published":false},"categories":[1],"tags":[],"class_list":["post-172","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"yoast_head":"\nMolecules in the Blood that Signal Self-Destruction - Josh Mitteldorf<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"Molecules in the Blood that Signal Self-Destruction\" \/>\n<meta property=\"og:description\" content=\"My theme the last few weeks has been the signals that trigger the body\u2019s self-destruction with age. \u00a0The easiest to target are molecules that circulate in the blood. \u00a0Last week, I covered a few that decrease in blood concentration as we age, and that cripple our defenses. \u00a0This week, I\u2019ll talk about signals that increase ... 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The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\\\/\\\/mathforum.org\\\/~josh\",\"sameAs\":[\"http:\\\/\\\/AgingAdvice.org\"],\"url\":\"https:\\\/\\\/scienceblog.com\\\/joshmitteldorf\\\/author\\\/joshmitteldorf\\\/\"}]}<\/script>\n<!-- \/ Yoast SEO Premium plugin. -->","yoast_head_json":{"title":"Molecules in the Blood that Signal Self-Destruction - Josh Mitteldorf","robots":{"index":"index","follow":"follow","max-snippet":"max-snippet:-1","max-image-preview":"max-image-preview:large","max-video-preview":"max-video-preview:-1"},"canonical":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/","og_locale":"en_US","og_type":"article","og_title":"Molecules in the Blood that Signal Self-Destruction","og_description":"My theme the last few weeks has been the signals that trigger the body\u2019s self-destruction with age. \u00a0The easiest to target are molecules that circulate in the blood. \u00a0Last week, I covered a few that decrease in blood concentration as we age, and that cripple our defenses. \u00a0This week, I\u2019ll talk about signals that increase ... Read more","og_url":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/","og_site_name":"Josh Mitteldorf","article_published_time":"2013-11-12T18:11:19+00:00","article_modified_time":"2014-04-23T23:10:22+00:00","author":"Josh Mitteldorf","twitter_card":"summary_large_image","twitter_misc":{"Written by":"Josh Mitteldorf","Est. reading time":"9 minutes"},"schema":{"@context":"https:\/\/schema.org","@graph":[{"@type":"Article","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/#article","isPartOf":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/"},"author":{"name":"Josh Mitteldorf","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/person\/214c5d1dad9f15c48f03128d5cfccdb1"},"headline":"Molecules in the Blood that Signal Self-Destruction","datePublished":"2013-11-12T18:11:19+00:00","dateModified":"2014-04-23T23:10:22+00:00","mainEntityOfPage":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/"},"wordCount":1793,"commentCount":1,"publisher":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#organization"},"inLanguage":"en-US","potentialAction":[{"@type":"CommentAction","name":"Comment","target":["https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/#respond"]}],"copyrightYear":"2013","copyrightHolder":{"@id":"https:\/\/scienceblog.com\/#organization"}},{"@type":"WebPage","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/","url":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/","name":"Molecules in the Blood that Signal Self-Destruction - Josh Mitteldorf","isPartOf":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#website"},"datePublished":"2013-11-12T18:11:19+00:00","dateModified":"2014-04-23T23:10:22+00:00","breadcrumb":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/#breadcrumb"},"inLanguage":"en-US","potentialAction":[{"@type":"ReadAction","target":["https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/"]}]},{"@type":"BreadcrumbList","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/2013\/11\/12\/molecules-in-the-blood-that-signal-self-destruction\/#breadcrumb","itemListElement":[{"@type":"ListItem","position":1,"name":"Home","item":"https:\/\/scienceblog.com\/joshmitteldorf\/"},{"@type":"ListItem","position":2,"name":"Molecules in the Blood that Signal Self-Destruction"}]},{"@type":"WebSite","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#website","url":"https:\/\/scienceblog.com\/joshmitteldorf\/","name":"Josh Mitteldorf","description":"Aging Matters","publisher":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#organization"},"potentialAction":[{"@type":"SearchAction","target":{"@type":"EntryPoint","urlTemplate":"https:\/\/scienceblog.com\/joshmitteldorf\/?s={search_term_string}"},"query-input":{"@type":"PropertyValueSpecification","valueRequired":true,"valueName":"search_term_string"}}],"inLanguage":"en-US"},{"@type":"Organization","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#organization","name":"Josh Mitteldorf","url":"https:\/\/scienceblog.com\/joshmitteldorf\/","logo":{"@type":"ImageObject","inLanguage":"en-US","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/logo\/image\/","url":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2024\/09\/1058476001.jpg","contentUrl":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-content\/uploads\/sites\/2\/2024\/09\/1058476001.jpg","width":864,"height":363,"caption":"Josh Mitteldorf"},"image":{"@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/logo\/image\/"}},{"@type":"Person","@id":"https:\/\/scienceblog.com\/joshmitteldorf\/#\/schema\/person\/214c5d1dad9f15c48f03128d5cfccdb1","name":"Josh Mitteldorf","image":{"@type":"ImageObject","inLanguage":"en-US","@id":"https:\/\/secure.gravatar.com\/avatar\/d3a8498f3d727156673030716d233edc57840f110d501b1b523e1780e9043b92?s=96&d=mm&r=g","url":"https:\/\/secure.gravatar.com\/avatar\/d3a8498f3d727156673030716d233edc57840f110d501b1b523e1780e9043b92?s=96&d=mm&r=g","contentUrl":"https:\/\/secure.gravatar.com\/avatar\/d3a8498f3d727156673030716d233edc57840f110d501b1b523e1780e9043b92?s=96&d=mm&r=g","caption":"Josh Mitteldorf"},"description":"Josh Mitteldorf studies evolutionary theory of aging using computer simulations. The surprising fact that our bodies are genetically programmed to age and to die offers an enormous opportunity for medical intervention. It may be that therapies to slow the progress of aging need not repair or regenerate anything, but only need to interfere with an existing program of self-destruction. Mitteldorf has taught a weekly yoga class for thirty years. He is an advocate for vigorous self care, including exercise, meditation and caloric restriction. After earning a PhD in astrophysicist, Mitteldorf moved to evolutionary biology as a primary field in 1996. He has taught at Harvard, Berkeley, Bryn Mawr, LaSalle and Temple University. He is presently affiliated with MIT as a visiting scholar. In private life, Mitteldorf is an advocate for election integrity as well as public health. He is an avid amateur musician, playing piano in chamber groups, French horn in community orchestras. His two daughters are among the first children adopted from China in the mid-1980s. Much to the surprise of evolutionary biologists, genetic experiments indicate that aging has been selected as an adaptation for its own sake. This poses a conundrum: the impact of aging on individual fitness is wholly negative, so aging must be regarded as a kind of evolutionary altruism. Unlike other forms of evolutionary altruism, aging offers benefits to the community that are weak, and not well focussed on near kin of the altruist. This makes the mechanism challenging to understand and to model. more at http:\/\/mathforum.org\/~josh","sameAs":["http:\/\/AgingAdvice.org"],"url":"https:\/\/scienceblog.com\/joshmitteldorf\/author\/joshmitteldorf\/"}]}},"jetpack_featured_media_url":"","jetpack_shortlink":"https:\/\/wp.me\/pgtN8h-2M","jetpack_sharing_enabled":true,"_links":{"self":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/172","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/users\/65"}],"replies":[{"embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/comments?post=172"}],"version-history":[{"count":0,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/posts\/172\/revisions"}],"wp:attachment":[{"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/media?parent=172"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/categories?post=172"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/scienceblog.com\/joshmitteldorf\/wp-json\/wp\/v2\/tags?post=172"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}