Thomas Dayspring
@Drlipid
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MD, FACP, FNLA - Clinical Lipidologist: Tweets/Re-Tweets do not represent endorsements/medical advice
Richmond, VA
Joined July 2009
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Can someone tell Rogan that the brain synthesizes all of its cholesterol and gets zero from the gut or from circulating in plasma lipoproteins. CLUELESS
Rogan confidently asserts that a “lack of cholesterol in the diet” is the primary theory of what causes alzheimer's disease
it is well known that americans rarely if ever eat chicken, eggs, pork, beef, fish, and dairy
i bet you don’t know anyone who eats these foods daily
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There are no words to say how proud I am that my great friend
@PeterAttiaMD
book "OUTLIVE" has hit # 1 on the NY Times Nonfiction Best Seller list (hardcover and e-book lists). If you have not got your copy yet, what are you waiting for?
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This paper is mandatory for those who want to better understand & then eliminate atherosclerosis. All including LDL deniers must realize that humans were never meant to harbor the LDLc (apoB) levels that are now commonplace. NORMAL LDL-C is 20-40 mg/dL
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A meta-analysis of 46 observational studies evaluating the association between statin therapy and the incidence of neuro-cognitive diseases showed that the use of statins not only did not increase the risk of f neurocognitive disorders, but rather was associated with a
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A masterpiece by
@maciejbanach
& colleagues of only 2-pages of which every line must be read. IF YOU FOLLOW ME - PROMISE TO READ ASAP - The paper so succinctly refutes every denier statement ever made. Free download
@nationallipid
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So simple - apoB-containing lipoproteins, when in excess numbers, easily pass thru the endothelium and deliver the necessary agent of atherogenesis - "cholesterol" to the arterial intima - that is when the maladaptive, chronic inflammatory process begins. Over time, first fatty
👉 Atherosclerosis is NOT an inflammatory condition
☝️Inflammation plays an important role, enhancing and accelerating the process, but the first and main driver is ApoB
👉Without ApoB, NO Atherosclerosis
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A phenomenal paper - always worth reading (line by line) for first time or re-reading, especially for deniers. Look how quickly plaque recedes (MOA shown) with apoB (LDLc) lowering.
@nationallipid
@society_eas
@TheFHFoundation
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No association of Egg Intake (≥7 egg/wk compared with <1 egg/wk intake) with blood lipids, CVD, and mortality in 177,000 People in 50 Countries
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For longevity - do we have a better rapamycin? Incredible review of SGLTi by James O'Keefe et al.
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There is no atherosclerosis without cholesterol in the arterial wall & only way it gets there is as a passenger in an apoB-containing lipoprotein - Early in life screening & using appropriate Rx is the way to prevent atherogenesis
@society_eas
@TheFHFoundation
@fhpatienteurope
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Way too many do not fully understand the concept of discordance among lipid (LDL-C & Non-HDL-C) & lipoprotein metrics (LDL-P & apoB). One cannot compare mg/dL (nmol/L) of each metric per se to each other, but one must look at which population percentile cut points the absolute
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Why is it such a hard concept for so many to understand that the arterial inflammation during atherogenesis is due to the immune response against the chronic invasion of PL & cholesterol carrying apoB particles that then aggregate & oxidize & get ingested by macrophages that
@MarkBrady2014
@Lpa_Doc
@Drlipid
@nationallipid
@SABOURETCardio
Mark, you don’t need inflammation to developing atherosclerosis. It’s an enhancer
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Labs often confuse patients by reporting reference ranges but do not show the at risk cut points. See below regarding apoB concentrations. Please be sure to request and check apoB when you are due for your next lipid panel.
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Not all LDLs are atherogenic. It is more accurate to say LDLs are POTENTIALLY atherogenic. Many serve their functional purpose & return their lipid contents to the liver (indirect RCT). If LDL-P (apoB) is ⬆️, LDLs can invade intima where many do induce atherogenesis
@society_eas
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Anyone using the terms good vs bad cholesterol or ratios thereof is a fraud who is nowhere close to being up to date on understanding lipid and lipoprotein metrics. There is not a single guideline or position statement anywhere that suggests raising HDL-C or correcting some ratio
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via
@NYTimes
If you want to get to know my colleague
@PeterAttiaMD
better, read this interview. Medicine 3.0 should be the norm and I am happy to be part of his team. Physicians have to step up their knowledge and approach.
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It still shocks me that with all of the apoB lowering therapies (all of which have CVOT data) that we now have clinicians, albeit a minority, still prescribing high dose statins. Compliance is dreadful. Patients do not want them. Easiest way to achieve goal is low dose statin
A 36% increased risk of high-intensity statins for inducing new onset diabetes as seen from all randomized, placebo-controlled trials (absolute increase from 3.5% to 4.8%).
🆕
@TheLancetEndo
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Do you really want to understand the Lipid Hypothesis? The following magnificent, incredibly enjoyable 5-part totally inclusive series written by David Steinberg in the Journal Of Lipid Research (open access) has long been forgotten. It was so important on my lipiddology
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Cholesterol Deniers BEWARE -
@PeterAttiaMD
just destroyed one of the silliest articles that deniers often quote
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"TO ARMS - TO ARMS" -- CITIZENS AND CLINICIANS OF THE WORLD - Beg borrow or steal to get this incredible new data from 100,000 people in the Copenhagen Study - The last 25 years of my teachings have been vindicated 😆. It is apoB alone - not LDL-C and for sure, not as so many
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Thanks🙌to my followers. By some miracle, I just acquired my 25K follower on Twitter, where I strive to provide serious lipid education (biochemistry, diagnostics, therapeutics & other complexities). My easily recognized illustrations are my trademark
@society_eas
@nationallipid
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I am incredibly proud to accept the
@nationallipid
Foundation's prestigious NLA 2023 NLA Clinician/Educator award at the Annual Meeting of the organization (June 2-4 in Atlanta - at which I will attend). This award honors NLA members who are respected / recognized by peer /
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Lipidaholics - Here is a treat for you - I have not done an in-person lecture for several years- Here is the video (with audio) of the actual animated PPT-presentation that I did last week at the prestigious International Conference on Nutrition in Medicine in Washinton DC. It
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Very happy to see what I have been teaching for 20 years is getting more and more recognition. ApoB is a more accurate marker of all-cause mortality risk in statin-Rx pts than LDL-C or non-HDL-C & apoB in addition is a more accurate marker of risk of MI than LDL-C.
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Why do so many confuse LDL (one of the human lipoprotein particles) with various laboratory derived metrics which characterize it such as LDL-C, non-HDL-C, LDL-P, apoB, LDL size, oxLDL, etc. Use proper terminology please. There is no such thing as an LDL-C particle !!! 😬
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This is one of the best lipid-related podcasts you will ever hear.
@PeterAttiaMD
interviews
@JohnKastelein
I was on the edge of y seat picking up so many pearls! Visit
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I have been trying to teach this for 25 years (apoB RULES) - The one sentence quote tells it all - All of these late events can be traced back to the retention of APOB LIPOPROTEINS within the arterial wall and then maladaptive local responses.
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I second that. His podcasts on lipids are like a lipidology textbook
Congrats to
@PeterAttiaMD
on his NLA Honorary Lifetime Membership Award - what an honor to have you as a lifetime member!
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Have received bunch of new followers so I am reposting my slide series: Understanding the standard lipid panel of Cholesterol & TG metrics. Remember the words of Lipid Godfathers - Fredrickson, Levy & Lees: lipid concentrations are simply surrogates of lipoprotein concentrations
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CLICK TO ENARGE - Since I find zero use for ten-year risk assessments, I have been asked many times for the "Dr Lipid" algorithm - for Dx of ASCVD risk & lipid Rx that I think judiciously applied would make ASCVD an orphan disease. Here it is (not tenable for all) -Put together
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The Effectiveness of Intermittent Fasting to Reduce Body Mass Index and Glucose Metabolism: A Systematic Review and Meta-Analysis
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Why are only an extreme minority of physicians and other clinicians testing for Lp(a), when 1 out of 5 humans will have abnormal concentrations?????? What is their excuse for not testing?
While elevated levels of LDL is known for heart disease, few know about Lp(a) risks. Elevated Lp(a) is an independent risk factor for cardiovascular disease. It should be detected early to help prevent CVD. Learn more:
#LpaAwarenessDay
#FHEurope
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Once again for my new viewers these graphics will help you navigate the standard Lipid Profile that most order and show that TC, LDL-C & Non-HDL-C are at best guesstimates (surrogates) of apoB. Less confusing to just order apoB. I advise both so as to not miss severe HTG
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If one is on a ketogenic diet, this is a scary poster - look at the ⬆️⬆️in LDL-C, in not only the lean folks but in everyone. Such a response suggests choosing a different diet. Ketogenic diet increases cellular cholesterol synthesis & down-regulates LDLR thus raising apoB
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These graphics reveal what any clinician & any at-risk patient (virtually all on the planet) & DENIERS need to know about ASCVD - ASCVD becomes an orphan disease at apoB < 50 mg/dL (LDL-P < 500-600 nmol/L)
@nationallipid
@society_eas
@TheFHFoundation
@fhpatienteurope
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Frst documented case of iron deficiency anemia due to the inhibition of iron absorption by turmeric. Because supplementation with turmeric is not only widespread it is important to be aware of this association
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This is an incredible open access Primary Prevention advice - Just about the best I have seen. ApoB oriented, no specific TG goal - although they should be tested or for sure no HDL-C goal. None of the absolute high-intensity statin silliness for primary prevention
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I am so proud to be part of Early Medical and work with my dear friend, the visionary
@PeterAttiaMD
- Time Magazine 2024 Top 100 Health List -
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The LDL-C and apoB deniers might want to carefully digest this study. In 2024, with few exceptions atherosclerosis and its consequences (MACE) are totally preventable: aggressive apoB & other risk factor control. SOONER RATHER THAN LATER
Very thought-provoking paper that builds on a lot of progress in the field of imaging and preventive cardiology
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It keeps raining (hard) on the deniers: UK BIOBANK analysis provides crucial insights regarding the effect of apoB & LDL-C levels on CV outcomes & underscores the importance of their reduction for improved CV health & mortality prevention.
@nationallipid
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Trust me - It is a big mistake not to listen (with pad and pen at hand) to the practice altering podcast:
@PeterAttiaMD
& world class nephrologist Rick Johnson: Fructose—The common link in high blood pressure, insulin resistance, T2D, & obesity?
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POST 2 OF 2 -- Periodically, as I acquire so many new followers, I re-post my basic "Understanding the Lipid Profile" graphic set.
@nationallipid
@society_eas
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Here is another paper that will rattle the bones of the apoB (and hence LDL and cholesterol) deniers. Authors conclude the MR screen identified APOB & lipoproteins containing APOB as CAUSAL DETERMINANTS of healthspan, a finding that is concordant with recent observations
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Well, well, well - DENIERS BEWARE - From the Washington Post comes "The better cholesterol test you did not know you needed" 25 years of my professional educational work starting to hit prime time. GET YOUR APOB TEST TODAY - If high never - ever - ignore it.
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Folks need to get real - Regarding al, the nonsensical statin hysteria that keeps popping up. As an internist with 37 years of private practice on my resume, I sadly signed many death certificates with ASCVD on line 1 yet never once signed a certificate with STATIN ADVERSITY on
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When it rains it pours: Another masterpiece that keeps putting nails in the coffins of those who deny the danger of LDL-cholesterol and apoB . Please make sure yours, and that of your loved ones is at or well beneath the guideline reccomendations. Ignore any other suggestions
👉Conquering cholesterol: a report from the front lines
☝️Strong genetic and observational data, along with the results of clinical lipid-lowering trials, have established the causal link between cholesterol and atherosclerosis. If the population maintained the cholesterol
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Shocker😂 - rosuvastatin 5 mg⬇️37.9% LDLc. The groups taking supplements - fish oil, cinnamon, garlic (actually raised LDLc), turmeric, plant sterols, or red yeast rice (p<0.001 had no benefit Published at
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Spencer is correct: I did four years of reduced carb (not ketogenic) with 5 days of severe fasting once a month (not especially fun) with 30 minutes of daily aerobics. I did it for 4 years. I pretty rapidly lost 70 pounds and maintained that loss during that period. After
I don’t know who needs to hear this but:
Keto
Intermittent fasting
Plant-based
Carnivore
Calorie counting
All fall under CICO (calories in, calories out)
When trying to lose weight, you have to eat fewer calories (eat less).
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Is this nutritional recommendation from WHO nonsense?: "to avoid piling on the pounds saturated fat should be < 10 % of diet" Notice what the man is drinking! Over 6 months I have lost 62 pounds with increasing fat on a low carb, w modified fast regimen
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Recently I said it was raining hard on the LDL deniers. Here is data that they are now facing a cyclone. Multivariable Mendelian randomization of APOB & LDL on healthspan suggests that the PREDOMINANT trait accounting for the relationship is APOB. In addition, preliminary
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Here is a 3-minute read from
@PeterAttiaMD
- Especially crucial for the apoB deniers - "Early action requires that each of us takes responsibility for engaging in decisions regarding our own health."
@nationallipid
@society_eas
@TheFHFoundation
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Planning a ketogenic diet? Review this preprint- as is known some get disastrous elevations in LDL-C & apoB (often not responsive to statins). Is it LDLR LOF, ⬆️cholesterol synthesis, or other unknown pre-existing gene issue?
@nationallipid
@society_eas
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Lipid/Lipoprotein Tutorial for the Day Part 3 - The liver can also directly secrete LDLs into plasma (normally ~40% of all LDLs during normal lipemia but slightly less when TG increase). Important to realize that not all LDLs are the by-products of VLDL lipolysis. During their
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How about this study (in press) - EZETIMIBE as a player to prevent Alzheimer's Disease and Related Dementia (ARRD). See Aging Biology | Ezetimibe lowers risk of Alzheimer’s and Related Dementias over 7-fold, reducing aggregation in model systems by inhibiting 14-3-3G::hexokinase
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Has been my experience that that many clinicians and patients would seriously fail this True or False test, but the slide title provides the correct answer! Will get into all of this in ensuing weeks.
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This may be the most important Tweet I have ever posted - If you do nothing else today, watch/listen to this podcast with the One and Only Allan Sniderman interviewed by
@PeterAttiaMD
Necessity for measuring apoB wil become obvious
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Here is an incredible article about LDL-C exposure over time and so sad it is firewalled for $40. Anyone advising patients about apoB or LDL-C should get this from their hospital library.
@nationallipid
@society_eas
@society_eas
@escardio
#cholesterol
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Just published in
@JACCJournals
was a SADLY not open-access paper on the 5 year data on the incredible ability of evolocumab in reducing MACE in ASCVD patients. Even better was the editorial which had this great graphic - they state - "prevention of ASCVD is a marathon - one
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I have had an influx of new followers, so I am reposting my slides on the basics of the Lipid Profile - The first slide tells you what the profile is not! Note TG & HDL-C are not goals of Rx. Next, see Part 2
@society_eas
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Lipidaholics who follow me know I am a stickler for proper scientific terminology. One of my peeves is the flagrant misuse of the term LDL which IS NOT an LDL metric (LDL-C, LDL-P). Please memorize this graphic
@nationallipid
@society_eas
@TheFHFoundation
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Optimal LDL-C (apoB), is about how low & how long. Recognize the importance of cumulative exposure to apoB particles. New saying is "lower is better AND earlier is better." Benefit & overall safety extends to very low levels.
@society_eas
@SethShayMartin
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Deniers. READ AND WEEP.
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This is such sad news and it is a shame The Nobel Committee never honored him. His work has reduced more CV morbidity and mortality that virtually any other
Dr Akiro Endo, discoverer of mevastatin that opened the way for one of the most effective methods to reduce risk of heart attack/stroke, died today at age 90. Impact to human health benefits is incalculable, it is estimated 200,000,000 people are on statins. You can read more
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Statins, pass thru cell membranes of all tissues (passively or via transporters), & reduce cholesterol synthesis in all cells (peripheral & brain) - (rarely disrupting cell functions). In the liver which needs substantial cholesterol, it causes significant up-regulation of LDLR
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POST 1 OF 2 -- Periodically, as I acquire so many new followers, I re-post my basic "Understanding the Lipid Profile" graphic set.
@nationallipid
@society_eas
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More potential future hope for Lp(a) patients - An Lp(a) disruptor. Open Access
Muvalaplin, a selective small molecule inhibitor of Lp(a) formation, was not associated with tolerability concerns and lowered Lp(a) levels up to 65% following daily administration for 14 days.
#ESCCongress
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A must read. Check your apoB and is elevated (>80 mg/dL) chase it (lower it) with a vengeance!
More lifespanning data on the crucial role of apolipoprotein B
@LancetLongevity
High apoB not so good: shortens lifespan, increases risks of CHD and stroke, and in multivariable analyses accounting for LDL-C, increases risk of type 2 diabetes.
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Great read: To Fight Fatty Liver, Avoid Sugary Foods& Drinks by
@anahadoconnor
An emerging public & individual health nightmare. My enzymes (elevated for decades) normalized rapidly on a reduced carb/intermittent fasting program as per
@PeterAttiaMD
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Why is this such a tough concept for so many to comprehend?
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Re the new NLA Lp(a) update - "Lp(a) is not consistently associated with baseline CAC and CAC progression, implying a distinct underlying pathobiology. Thus, a CAC score of ZERO (0) DOES NOT ELIMINATE THE RISK associated with elevated Lp(a), particularly in younger adults, in
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Must reading by any of the ketogenic LDL response deniers - one is playing with their lives by ignoring the apoB (LDL-C) response that often occurs. One has 2 choices - switch to a different diet or get on apoB lowering therapy
AHA starts tomorrow- lots of material on Lp(a), will cover as we go....
Keto is also on menu:
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Carbs have been vilified & blamed for obesity epidemic, T2D & CVD. But the important role of carbohydrate in a healthy diet is often forgotten. This paper is an excellent review of carbs re wt, IR, T2D, inflammation, lipids, CVD & all-cause mortality.
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Easiest way to spot someone not fully knowledgeable with lipids is how they speak/tweet re lipid metrics (tests). LDL, HDL, VLDL, Lp(a) ARE NOT LAB TESTS - they are lipoproteins. If one wants to discuss their metrics - One needs to use proper terms
@society_eas
@nationallipid
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Luckily when active I have been in very advanced practices. Recently I was asked "what is my current "treatment algorithm" recommendation. Here are both my risk assessment and treatment advice. I realize the vast majority of clinicians (sadly) are not doing sterol markers and not
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LDLs are not inherently atherogenic: LDLs may or may not be atherogenic. If they return their cholesterol mass (LDLc) to the liver (indirect RCT) that is beneficial & not atherogenic. If BECAUSE OF ⬆️ concentrations (LDL-P, apoB) LDLs enter the artery they can be atherogenic
@Drlipid
@society_eas
@nationallipid
So is it reasonable to assert that LDL-C is inherently atherogenic or is that an oversimplification?
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Gross negligence not to check Lp(a) in yourself, in your loved ones and of course in all patients. At present time it is pretty much a once per lifetime test
Are you the one? If you have high Lp(a), you could be walking around at risk for a heart attack and not know it. You can
#KnowLpa
and get ahead of heart disease.
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CLICK - Over the next several days & weeks I will be sharing many teaching slides delving into enigmatic world of High Density Lipoproteins. Pictures are helpful, but ultimately advanced reading is required - Warning: much of what we have been taught about HDL is erroneous
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75-85% of the potentially absorbable gut pool of free cholesterol is of ENDOGENOUS origin (enters gut via biliary system) & only 15-25 % of that pool is from diet. In those with normal NPC1L1 & ABCG5/G8 function. INGESTED cholesterol has little clinical effect on LDL metrics
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@CarnivoreMD
@DBelardoMD
So the rest of the world, including every CV organization statement on apoB-containing particles is missing everything you see so clearly. Where can we look to acquire your wisdom?
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My Understanding ApoE talk is now up for viewing - info not easy to find - so when you have 1 hour & 15 minutes for apolipoproteins, pour a big glass of wine, find a nice seat and learn
@nationallipid
@society_eas
Go to and scroll down to SELA section
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Reminder: THERE IS NO LAB TEST called LDL. LDL refers to a heterogenous group of the lipoprotein family defined by a specific density range. LDL-C IS NOT A LIPOPROTEIN but rather a lab metric that provides the collective cholesterol cargo of all LDLs per unit volume
@society_eas
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Therapeutic Potential of Ketone Bodies for patients with CVD
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Long overdue
Some cardiologists are suggesting that it's time to abandon LDL as the best cholesterol test for heart disease risks:
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@GregorGl
@PeterAttiaMD
@MohammedAlo
Big mistake - Do not wait for atherosclerosis to be present- If risk factors exist treatment is needed long before plaque is visible - That is termed primordial prevention. See
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Sadly - A majority of persons who should be on lipid modulating drugs in both primary and secondary prevention scenarios have not been started on lipid Rx - that is solely due to physicians not being well schooled in understanding lipid/lipoprotein mediated CV-risk.
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President Biden had annual exam today and resuts were released to the public. He has chronic AFib with normal echo (taking apixaban). He has hyperlipidemia and is on rosuvastatin (dose not specified): his lipid panel is below: no apoB - I guess his plan did not cover it 😄
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A Sniderman et al masterpiece - Mass of cholesterol that will be deposited in artery is determined by the # of apoB particles that are trapped within intima. # of apoB particles that enter is determined primarily by the # of circulating apoB particles
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Studies have not demonstrated an increased risk of cognitive impairment, Alzheimer's dementia, or hemorrhagic stroke associated with lowering LDL-C levels. The concerns about stroke and cognitive issues with very low LDL-C levels have been refuted. See LDL Cholesterol Lowering:
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A9: Numerous clinical trials have demonstrated that there is no danger in lowering plasma LDL-C too low. LDL-C is the cholesterol circulating in plasma and is not a measure of tissue cholesterol (all cells synthesize all the cholesterol they need): LDL-C has no relation to brain,
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Provocative Commentary by
@PeterAttiaMD
re the REDUCE IT Trial is well worth a read - I find it hard to argue with his analysis. Ideally, another trial with corn oil (or other inert placebo) vs EPA vs EPA/DHA.
@society_eas
@nationallipid
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From the NLA ApoB Consensus statement is the useful info about the population percentile cut points for cholesterol and apoB concentration metrics. A copy of this belongs on every clinician's desk
@nationallipid
@society_eas
@escardio
@atherosociety
@TheFHFoundation
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Not knowing about Lp(a) is an indictment of the medical profession & criminal for a cardiologist. In 2023, how can it be that clinicians are unaware of a major, genetic cause of ASCVD & CAVS. Do they not read, obtain CME, talk to colleagues?
•
#Lpa
tests are rarely performed even in patients w/ ⬆️ CV risk
• Lp(a) testing is associated w/ more intensive treatment and ⬇️☠️
• Lp(a) testing is an opportunity to 💪
#ASCVD
prevention
#FindLpa
#KnowLpa
@fhpatienteurope
@society_eas
@EASCongress
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Have to take a time out and THANK ALL MY FRIENDS & FOLLOWERS who now have now exceeded the 30K mark. Pretty good for an old lipidologist (51 years as a physician) who still loves (now globally) to illustrate & teach lipids & lipoproteins.
@nationallipid
@society_eas
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MUST READ - Official AHA Statement on Lp(a) - endorsed by
@atherosociety
Call and demand that your lab reports the concentration in nmol/L - stop accepting the value in mg/dL (conversion of which is inaccurate).
@society_eas
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As usual a fantastic article suggested by
@drpablocorral
and I hope all note that on this graphic from the paper, the oxidation of the LDL particle occurs WITHIN the wall of the artery NOT in plasma - it is a total waste of money to order the oxLDL test. Also recognize this
👉Response to retention hypothesis as a source of targets for arterial wall-directed therapies to prevent atherosclerosis: A critical review
☝️Atherogenesis begins with the trapping of apolipoprotein-B-containing lipoproteins to modified glycosaminoglycan chains
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Cholesterol (of which there is ONLY one type) is needed by cells in very small concentrations: too much is harmful and can kill the cell. We do not (cannot) measure cell cholesterol levels but rather that carried within various cholesterol carrying particles (lipoproteins) in our
@Drlipid
Tom - what do you propose we say? Calling it atherogenic cholesterol will sail over the heads of many. Maybe plaque-forming cholesterol? Advice welcome!
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I cannot shout this loud enough - if your clinician downplays lipid abnormalities - WITH RESPECT TO LIPID CARE, YOU MUST BE YOUR OWN ADVOCATES. Get a second opinion. Follow
@nationallipid
&
@society_eas
&
@TheFHFoundation
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Lifelong elevated concentrations of LDL-C (apoB) have already sown the seeds of atherosclerosis in millions of people, increasing their risk for ASCVD
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(GOOD CHOLESTEROL 😂) Despite decades of belief that HDL protects from ASCVD, human genetic studies & failure of several measures that raise HDLc to reduce ASCVD events—have called into question the protective effect of HDL (at least as reflected by HDLc)
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Sagan was a prophet, and we have all seen and have to deal with the pseudoscience and science deniers as they spread their nonsense
📕In 1995, American astronomer Carl Sagan predicted what a future American society could look like.
His forecast has proven prescient. Read below.
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