Alonzo Leroy Landy, 32, was fatally shot by law enforcement officials in Fayette County, Georgia, USA, according to multiple American news reports and a statement from Georgia officials. A statement from the Georgia Bureau of Investigation said, “On Sunday, November 29, 2020, the GBI was requested by the Fayette County Sheriff’s Office to conduct an […]

An uplifting Happy Father’s Day slideshow video — featuring a number of fathers and their children — was created by 13-year-old Essien Douglas, who runs the YouTube channel Emoney Extreme TV. Shown as part of the special Father’s Day broadcast hosted by his dad Dr Ty Douglas, the song used in the video was written […]

The latest design in Bernews’ weekly Wallpaper Wednesday takes a captivating dive into Bermuda’s rich history, with a rendition of the Sea Venture shipwreck, Bermuda’s national motto, ‘Quo Fata Ferunt’ and the Bermuda Triangle. The design is available in two sizes; a Facebook profile cover image and also in a vertical format, ideally sized for […]

The Bermuda Police Service [BPS] is “renewing the witness appeal for anyone that can assist with the ongoing investigation regarding a single vehicle motorcycle collision that claimed the life of 50-year-old Steve Perinchief, Bermuda’s fifth road fatality this year.” A police spokesperson said, “In particular, members of the public who can confirm Mr. Perinchief’s whereabouts […]

An 18-year-old male has been charged in connection with the fatal stabbing of 20-year-old Zijae Jones, which occurred at Horseshoe Bay Beach on Bermuda Day Dahny Simmons-Outerbridge, of Warwick, was charged with killing Zijae Jones. He was also charged with being in possession of a knife in a public place. Simmons-Outerbridge was not required to enter a […]

Date: November 10, 2024

Location: Estonia, Finland, Iceland, Sweden

Tags:

How to build muscle and loose fat at the same time.

By: Tim Ernst

Is it possible to gain muscle while at the same time loose fat? Some argue that you either have to do one or the other. I'm here to tell you that it is possible, but the secret is all about nutrient timing.

There are certain times of the day when you want to be in a caloric surplus. The only way to build muscle is to be in a caloric surplus and the only way to loose fat is to be in a caloric deficit. How do you do both at the same time?

Research shows that your most optimal time for muscle growth is what you consume after your workout. If you are not consuming enough calories after your workout, then you are just wasting your time.

Here is an example on how to start your day.

8:00 am: Low-carb protein shake with a greens product.

10:30 am: 2eggs plus 4 whites scrambled with cheese, spinach, onions, peppers, and mushrooms.

1:00 pm: 2 oz of dry roasted nuts.

3:00 pm: Chicken Breast with sweet potato or brown rice.

5:00 pm (workout) Consume your a favorite pre workout shake if you want for energy but, it's not necessary.

5:30 pm 30 minutes into your workout consume a high carb drink like Karbolyn, Power Carb, or Vitargo.

5:45 pm (immediately post-workout): quickly digested protein/carb beverage.

6:15pm: 2 oz of pasta (dry weight); 4 oz of Ground Turkey mixed with egg whites.; 2 slices of 12-grain bread; package of broccoli or green beans.

7:45 pm: 1 cup brown rice, cous cous, or quinoa 4 oz of chicken breast; 2 slices of 12-grain bread, asparagus.

10:00 pm: Hand full of mixed nuts or avocado and fish oils.

That's it!

Get ready to GROW.

Fat Bear Week



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With summer in full swing, the National Fire Protection Association (NFPA) and Electrical Safety Foundation International (ESFI) are joining forces to remind people about the potential electrical hazards in swimming pools, hot tubs and spas, on board boats and in the waters surrounding boats, marinas and launch ramps.

New on Kink Men: Colt Spence has had a terrible morning. It’s taking him longer than he anticipated to complete an endeavor that required him to report to work on a Sunday to try and wrap it up. Fortunately, the workshop is situated close to the bus station in the heart of town, and Colt... View Article

The post Kink Men: Carter Collins and Colt Spence – “Big Fat Man Meat” appeared first on QueerClick.

Television distorts, mocks and marginalizes fat people. Fat characters are reduced to caricatures whose stories and identities aren’t developed and don’t matter. In one study by Tzoutzou et al., all 36 compliments about appearance given to women were for thin women. Not one positive message was included for a woman of an average or overweight […]

Paperback, Hardcover, Kindle, Audiobook – July 9, 2013

By Keegan Kelly Published: November 11th, 2024

In the documentary, Martha Stewart opens up about her childhood and the complicated relationship she had with her father.

The seed for the current project was sown last year when a similarly-themed exposition was given pride of place at the Bundestag, the German parliament building in Berlin.

The following article, It’s Election Day, But the Fat Lady Isn’t Singing Yet, was first published on The Black Sphere.

Photo Credit: Michigan Advance Shards of 2022 In the 2022 Midterm Election, the political soothsayers were predicting a huge ‘red wave’ was going to sweep over America akin to the 1994 Gingrich Revolution and the 2010 Tea Party Revolt.  However, writing in a previous article, we made a different prediction that went against the conventional …

Continue reading It’s Election Day, But the Fat Lady Isn’t Singing Yet ...

It is an embarrassing critique for Hamas, which has used religious arguments to justify its actions.

Sinwar’s death does not make Hamas–Fatah reconciliation more likely, whoever his successor may be Expert comment jon.wallace 22 October 2024

The killing may aid Hamas recruitment – but it will not make agreement with Fatah any easier to achieve.

Western political leaders were quick to argue that Israel’s killing of Hamas leader Yahya Sinwar on 17 October presented an opportunity for a ceasefire in Gaza and the return of Israeli hostages.

US President Joe Biden immediately called on Israeli prime minister Benjamin Netanyahu to seize the moment to negotiate, now that Israel has achieved one of its war aims.

However, that ‘moment’ has already passed. Israel’s military assault on Gaza has intensified since Sinwar was killed, leading UN Peace Process Co-ordinator Tor Wennesland to say that ‘nowhere is safe in Gaza’. It is abundantly clear Netanyahu is intent on further degrading Hamas, resetting a new ‘power balance’ and carving out a buffer zone, no matter the cost in Palestinian lives or Israeli hostages. 

But there are other implications of Sinwar’s assassination beyond the zero-sum analysis of will there or won’t there be a ceasefire.

Hamas’s ability to fight

At present, everyone has an opinion on how Sinwar’s killing will affect Hamas and its ability to resist and respond to Israel’s military. His death will have been a major blow – symbolically, operationally, and psychologically. Hamas has been downgraded and its capacity to respond compromised.

But it will recover, regenerate and retaliate in time – and Sinwar’s death will have been no surprise to Palestinians in Gaza or elsewhere. Hamas is accustomed to seeing its leaders assassinated. Since its formation in 1987, it has been ‘decapitated’ many times, only to continue with its mission to ‘liberate Palestine’.

Hamas’s portrayal of Sinwar dying in his fatigues, head wrapped in a keffiyeh and resisting until the end will persuade many young Palestinians that he died as a martyr serving the Palestinian cause. Many will be inspired to join and fortify the ranks of Hamas as a result.

The IDF’s release of drone footage showing Sinwar’s last moments will have done nothing to undermine his credibility. 

On the contrary, it will serve as a rallying call to disaffected and disenfranchised young Palestinians horrified by Israel’s bombing of civilian targets in Gaza and disaffected with Fatah’s inability to prevent Israeli settler expansion and violence in the West Bank.

Reconciliation

Some hope that if Sinwar is replaced by a more ‘moderate’ leader, his killing may smooth the path to Hamas–Fatah reconciliation – and that this could provide a foundation for a patchwork political solution when Israel and Gaza arrive at the ‘day after.’  

But the idea that a downgraded and ‘leaderless’ Hamas will be susceptible to international pressure to reconcile with Fatah is divorced from reality.  

Prospective new Hamas leaders such as Khaled al Meshaal and Khalil al-Hayya are based in Qatar. 

They may be more pliable to external pressure to reconcile with Fatah in search of a political outcome, but their ability to influence events on the ground in Gaza will be limited. That was demonstrated by the Sinwar-orchestrated attacks on 7 October 2023, which took place without the blessing of the exiled leadership in Doha.

Hamas has long gone to ground in Gaza and become far more decentralized than it was before 7 October. It is now more typical of an insurgency, where Hamas cadres exercise a great degree of operational autonomy.

In other words, the disconnect between Hamas in Gaza and its political leadership in Qatar has only grown wider since this round of conflict started.

International efforts

That will undermine international efforts made by Qatar, Egypt, Saudi Arabia, China, Russia and others to bring about a reconciliation. Moscow and Beijing already hosted reconciliation talks in February and April early this year but made no progress in closing the chasm between the two parties. Saudi Arabia has also hosted talks.

The three Arab states, none of which have so far commented publicly on Sinwar’s killing, will likely view his death as an opportunity to bolster the political wing of Hamas – backing it with pledges of political, diplomatic and financial support.

Saudi Arabia and Egypt will have next to no influence over the succession process, but Qatar’s long-established relationship with the political wing of Hamas affords it leverage over the organization, albeit limited. They may be able to strengthen the hand of those based in Doha by promising to work harder at securing a ceasefire, guaranteeing the provision of humanitarian relief, and working towards a political solution.

James M. Ntambi
Sep 1, 1999; 40:1549-1558
Reviews

Gijs den Besten
Sep 1, 2013; 54:2325-2340
Reviews

K Schoonjans
May 1, 1996; 37:907-925
Reviews

Robert W. Mahley
Jan 1, 1999; 40:1-16
Reviews

William R. Morrison
Oct 1, 1964; 5:600-608
Articles

seveni.1999 posted a photo:

seveni.1999 posted a photo:

A father who pleaded guilty to sexually molesting his 13-year-old daughter was sentenced to several years of imprisonment in the St Catherine Circuit Court on Tuesday.

Sirtuin 6, SIRT6, is critical for both glucose and lipid homeostasis and is involved in maintaining genomic stability under conditions of oxidative DNA damage such as those observed in age-related diseases. There is an intense search for modulators of SIRT6 activity, however, not many specific activators have been reported. Long acyl-chain fatty acids have been shown to increase the weak in vitro deacetylase activity of SIRT6 but this effect is modest at best. Herein we report that electrophilic nitro-fatty acids (nitro-oleic acid and nitro-conjugated linoleic acid) potently activate SIRT6. Binding of the nitro-fatty acid to the hydrophobic crevice of the SIRT6 active site exerted a moderate activation (2-fold at 20 μm), similar to that previously reported for non-nitrated fatty acids. However, covalent Michael adduct formation with Cys-18, a residue present at the N terminus of SIRT6 but absent from other isoforms, induced a conformational change that resulted in a much stronger activation (40-fold at 20 μm). Molecular modeling of the resulting Michael adduct suggested stabilization of the co-substrate and acyl-binding loops as a possible additional mechanism of SIRT6 activation by the nitro-fatty acid. Importantly, treatment of cells with nitro-oleic acid promoted H3K9 deacetylation, whereas oleic acid had no effect. Altogether, our results show that nitrated fatty acids can be considered a valuable tool for specific SIRT6 activation, and that SIRT6 should be considered as a molecular target for in vivo actions of these anti-inflammatory nitro-lipids.

In addition to their well-known role in the control of cellular proliferation and cancer, cell cycle regulators are increasingly identified as important metabolic modulators. Several GWAS have identified SNPs near CDKN2A, the locus encoding for p16INK4a (p16), associated with elevated risk for cardiovascular diseases and type-2 diabetes development, two pathologies associated with impaired hepatic lipid metabolism. Although p16 was recently shown to control hepatic glucose homeostasis, it is unknown whether p16 also controls hepatic lipid metabolism. Using a combination of in vivo and in vitro approaches, we found that p16 modulates fasting-induced hepatic fatty acid oxidation (FAO) and lipid droplet accumulation. In primary hepatocytes, p16-deficiency was associated with elevated expression of genes involved in fatty acid catabolism. These transcriptional changes led to increased FAO and were associated with enhanced activation of PPARα through a mechanism requiring the catalytic AMPKα2 subunit and SIRT1, two known activators of PPARα. By contrast, p16 overexpression was associated with triglyceride accumulation and increased lipid droplet numbers in vitro, and decreased ketogenesis and hepatic mitochondrial activity in vivo. Finally, gene expression analysis of liver samples from obese patients revealed a negative correlation between CDKN2A expression and PPARA and its target genes. Our findings demonstrate that p16 represses hepatic lipid catabolism during fasting and may thus participate in the preservation of metabolic flexibility.

Oxygen regulates hypoxia-inducible factor (HIF) transcription factors to control cell metabolism, erythrogenesis, and angiogenesis. Whereas much has been elucidated about how oxygen regulates HIF, whether lipids affect HIF activity is un-known. Here, using cultured cells and two animal models, we demonstrate that lipoprotein-derived fatty acids are an independent regulator of HIF. Decreasing extracellular lipid supply inhibited HIF prolyl hydroxylation, leading to accumulation of the HIFα subunit of these heterodimeric transcription factors comparable with hypoxia with activation of downstream target genes. The addition of fatty acids to culture medium suppressed this signal, which required an intact mitochondrial respiratory chain. Mechanistically, fatty acids and oxygen are distinct signals integrated to control HIF activity. Finally, we observed lipid signaling to HIF and changes in target gene expression in developing zebrafish and adult mice, and this pathway operates in cancer cells from a range of tissues. This study identifies fatty acids as a physiological modulator of HIF, defining a mechanism for lipoprotein regulation that functions in parallel to oxygen.

Elisa Vidal
Dec 1, 2020; 61:1733-1746
Research Articles

Thibaut Bourgeois
Dec 11, 2020; 0:jlr.RA120000737v1-jlr.RA120000737
Research Articles

Photoreceptors have high energy-demands and a high density of mitochondria that produce adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) of fuel substrates. Although glucose is the major fuel for central nervous system (CNS) brain neurons, in photoreceptors (also CNS), most glucose is not metabolized through OXPHOS but is instead metabolized into lactate by aerobic glycolysis. The major fuel sources for photoreceptor mitochondria remained unclear for almost six decades. Similar to other tissues (like heart and skeletal muscle) with high metabolic rates, photoreceptors were recently found to metabolize fatty acids (palmitate) through OXPHOS. Disruption of lipid entry into photoreceptors leads to extracellular lipid accumulation, suppressed glucose transporter expression, and a duel lipid/glucose fuel shortage. Modulation of lipid metabolism helps restore photoreceptor function. However, further elucidation of the types of lipids used as retinal energy sources, the metabolic interaction with other fuel pathways, as well as the crosstalk among retinal cells to provide energy to photoreceptors is not yet known. In this review, we will focus on the current understanding of photoreceptor energy demand and sources, and potential future investigations of photoreceptor metabolism.

Genetic variants that increase the risk of fatty liver disease (FLD) and cirrhosis have recently been identified in the proximity of membrane bound O-acyltransferase domain-containing 7 (MBOAT7).  To elucidate the link between these variants and FLD we characterized Mboat7 liver-specific knock-out mice (Mboat7-LSKO).  Chow-fed Mboat7-LSKO mice developed fatty livers and associated liver injury.  Lipidomic analysis of liver using mass spectrometry revealed a pronounced reduction in 20-carbon polyunsaturated fatty acid content in phosphatidylinositols (PIs), but not in other phospholipids. The change in fatty acid composition of PIs in these mice was associated with a marked increase in de novo lipogenesis due to activation of SREBP-1c, a transcription factor that coordinates the activation of genes encoding enzymes in the fatty acid biosynthesis pathway. Hepatic removal of both SREBP cleavage activating protein (Scap) and Mboat7 normalized hepatic triglycerides relative to Scap only hepatic knock-out showing increased SREBP-1c processing is required for Mboat7 induced steatosis.  This study reveals a clear relationship between PI fatty acid composition and regulation of hepatic fat synthesis and delineates the mechanism by which mutations in MBOAT7 cause hepatic steatosis.

Recent studies have highlighted an important role for lysophosphatidylcholine acyltransferase 3 (LPCAT3) in controlling the PUFA composition of cell membranes in the liver and intestine. In these organs, LPCAT3 critically supports cell membrane-associated processes such as lipid absorption or lipoprotein secretion. However, the role of LPCAT3 in macrophages remains controversial. Here, we investigated LPCAT3’s role in macrophages both in vitro and in vivo in mice with atherosclerosis and obesity. To accomplish this, we used the LysMCre strategy to develop a mouse model with conditional Lpcat3 deficiency in myeloid cells (Lpcat3KOMac). We observed that partial Lpcat3 deficiency (approx. 75% reduction) in macrophages alters the PUFA composition of all phospholipid (PL) subclasses, including phosphatidylinositols and phosphatidylserines. A reduced incorporation of C20 PUFAs (mainly arachidonic acid [AA]) into PLs was associated with a redistribution of these FAs toward other cellular lipids such as cholesteryl esters. Lpcat3 deficiency had no obvious impact on macrophage inflammatory response or endoplasmic reticulum (ER) stress; however, Lpcat3KOMac macrophages exhibited a reduction in cholesterol efflux in vitro. In vivo, myeloid Lpcat3 deficiency did not affect atherosclerosis development in LDL receptor deficient mouse (Ldlr-/-) mice. Lpcat3KOMac mice on a high-fat diet displayed a mild increase in hepatic steatosis associated with alterations in several liver metabolic pathways and in liver eicosanoid composition. We conclude that alterations in AA metabolism along with myeloid Lpcat3 deficiency may secondarily affect AA homeostasis in the whole liver, leading to metabolic disorders and triglyceride accumulation.

Sphingolipids have become established participants in the pathogenesis of obesity and its associated maladies. Sphingosine kinase 1 (SPHK1), which generates S1P, has been shown to increase in liver and adipose of obese humans and mice and to regulate inflammation in hepatocytes and adipose tissue, insulin resistance, and systemic inflammation in mouse models of obesity. Previous studies by us and others have demonstrated that global sphingosine kinase 1 KO mice are protected from diet-induced obesity, insulin resistance, systemic inflammation, and NAFLD, suggesting that SPHK1 may mediate pathological outcomes of obesity. As adipose tissue dysfunction has gained recognition as a central instigator of obesity-induced metabolic disease, we hypothesized that SPHK1 intrinsic to adipocytes may contribute to HFD-induced metabolic pathology. To test this, we depleted Sphk1 from adipocytes in mice (SK1^fatKO) and placed them on a HFD. In contrast to our initial hypothesis, SK1^fatKO mice displayed greater weight gain on HFD and exacerbated impairment in glucose clearance. Pro-inflammatory cytokines and neutrophil content of adipose tissue were similar, as were levels of circulating leptin and adiponectin. However, SPHK1-null adipocytes were hypertrophied and had lower basal lipolytic activity. Interestingly, hepatocyte triacylglycerol accumulation and expression of pro-inflammatory cytokines and collagen 1a1 were exacerbated in SK1^fatKO mice on a HFD, implicating a specific role for adipocyte SPHK1 in adipocyte function and inter-organ cross-talk that maintains overall metabolic homeostasis in obesity. Thus, SPHK1 serves a previously unidentified essential homeostatic role in adipocytes that protects from obesity-associated pathology. These findings may have implications for pharmacological targeting of the SPHK1/S1P signaling axis.

Spatial changes of FAs in the retina in response to different dietary n-3 formulations have never been explored, although a diet rich in EPA and DHA is recommended to protect the retina against the effects of aging. In this study, Wistar rats were fed for 8 weeks with balanced diet including either EPA-containing phospholipids (PLs), EPA-containing TGs, DHA-containing PLs, or DHA-containing TGs. Qualitative changes in FA composition of plasma, erythrocytes, and retina were evaluated by gas chromatography-flame ionization detector. Following the different dietary intakes, changes to the quantity and spatial organization of PC and PE species in retina were determined by LC coupled to MS/MS and MALDI coupled to MS imaging. The omega-3 content in the lipids of plasma and erythrocytes suggests that PLs as well as TGs are good omega-3 carriers for retina. However, a significant increase in DHA content in retina was observed, especially molecular species as di-DHA-containing PC and PE, as well as an increase in very long chain PUFAs (more than 28 carbons) following PL-EPA and TG-DHA diets only. All supplemented diets triggered spatial organization changes of DHA in the photoreceptor layer around the optic nerve. Taken together, these findings suggest that dietary omega-3 supplementation can modify the content of FAs in the rat retina.

S-Acylation, a reversible post-translational lipid modification of proteins, controls the properties and function of various proteins, including ion channels. Large conductance Ca2+-activated potassium (BK) channels are S-acylated at two sites that impart distinct functional effects. Whereas the enzymes that attach lipid groups are known, the enzymes mediating lipid removal (i.e. deacylation) are largely unknown. Here, McClafferty et al. identify two enzymes, ABHD17a and ABHD17c, that excise BK channel lipid groups with remarkable precision. These findings lend insights into mechanisms that orchestrate the (de)acylation that fine-tunes ion channel function in physiology and disease.

The increasing consumption of high-fat foods combined with a lack of exercise is a major contributor to the burden of obesity in humans. Aerobic exercise such as running is known to provide metabolic benefits, but how the over-consumption of a high fat diet (HFD) and exercise interact is not well characterized at the molecular level. Here, we examined the plasma proteome in mice for the effects of aerobic exercise as both a treatment and as a preventative regime for animals on either HFD or a healthy control diet. This analysis detected large changes in the plasma proteome induced by the HFD, such as increased abundance of SERPINA7, ALDOB, and down-regulation of SERPINA1E, CFD (adipsin). Some of these changes were significantly reverted using exercise as a preventative measure, but not as a treatment regime. To determine if either the intensity, or duration, of exercise influenced the outcome, we compared high-intensity interval training (HIIT) and endurance running. Endurance running slightly out-performed HIIT exercise, but overall, both provided similar reversion in abundance of plasma proteins modulated by the high-fat diet including SERPINA7, APOE, SERPINA1E, and CFD. Finally, we compared the changes induced by over-consumption of HFD to previous data from mice fed an isocaloric high saturated fat (SFA) or polyunsaturated fat (PUFA) diet. This identified several common changes including increased APOC2 and APOE, but also highlighted changes specific for either over-consumption of HFD (ALDOB, SERPINA7, CFD), SFA-based diets (SERPINA1E), or PUFA-based diets (Haptoglobin - Hp). Together, these data highlight the importance of early intervention with exercise to revert HFD-induced phenotypes and suggest some of the molecular mechanisms leading to the changes in the plasma proteome generated by high fat diet consumption. Web-based interactive visualizations are provided for this dataset (larancelab.com/hfd-exercise), which give insight into diet and exercise phenotypic interactions on the plasma proteome.

Mysterious black balls that washed up on Sydney, Australia, beaches were initially suspected to be tar balls but turned out to be miniature "fatbergs" containing human feces.

The fate of fictional Montana Gov. John Dutton -- played by Kevin Costner -- has finally been disclosed in the Season 5B premiere of "Yellowstone" that aired on Paramount Sunday night.

Nov. 12—Jarrett Gronski wasn't expecting to cry the morning before playing Wayne State. Like most athletes, the Bemidji State football team's senior running back has his pregame rituals. But that routine shook out a little differently before the Beavers' game against the Wildcats. John Gronski — Jarrett's father and a prolific running back for BSU back in the late 1980s — was officially ...

In 1619, George Yeardley, the newly appointed governor of Jamestown, made history: He convened 22 elected members of a burgeoning commonwealth, creating the first democratic assembly in America.

Artist Abbot Thayer illustrated the prevalence of camouflage in the animal world and advocated using it as a military tactic

The grand buildings of Washington, D.C. would look quite different were it not for the work of Palladio. Read more at Smithsonian.com

Photographer Drew Gardner has a passion for history. His long-term project, “The Descendants,” (https://www.drewgardner.com/descendants)  wherein he recreates famous portraits of historical figures featuring their direct offspring, is his most visible expression of this interest. But like a lot of people who study history, Gardner has in recent years begun to contemplate more deeply the question of whose stories have been judged worthy of preservation, and whose have been allowed to fade into obscurity. That was how he decided to shift his specific focus to locating and photographing Black American descendants of Civil War veterans. You can take a look at Gardner’s photographs and read magazine editor Jennie Rothenberg Gritz’s exploration of their meaning here (https://www.smithsonianmag.com/history/descendants-black-civil-war-heroes-wear-heritage-pride-180983397/) . On the latest episode of the Smithsonian podcast “There’s More to That,” (https://www.smithsonianmag.com/podcast)  I speak with Janisse Flowers and her 9-year-son, Neikoye, who are descended from the Civil War drummer boy David Miles Moore Jr. After some reflection, Janisse and her husband decided to grant Gardner’s request to photograph Neikoye dressed in a replica of Moore’s Union Army uniform. Both Janisse and Neikoye share their surprise over how this experience made them more conscious of their heritage. I’m also joined by Gardner himself, who describes the challenges—and, he hopes, the potential benefits—of asking Black Americans to revisit one of the most painful chapters of America’s history by (almost) literally stepping into their ancestors’ shoes. You can learn more about Drew and his work at his website (https://www.drewgardner.com/) . Find prior episodes of our show here (https://www.smithsonianmag.com/podcast/) . There’s More to That is a production of Smithsonian magazine and PRX Productions. From the magazine, our team is Chris Klimek, Debra Rosenberg and Brian Wolly. From PRX, our team is Jessica Miller, Adriana Rosas Rivera, Genevieve Sponsler, Terence Bernardo, and Edwin Ochoa. The Executive Producer of PRX Productions is Jocelyn Gonzales. Fact-checking by Stephanie Abramson. Episode artwork by Emily Lankiewicz. Music by APM Music.